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THE UNIVERSITY OF ALBERTA 


1. EFFECTS OF PROXIIIAL VERSUS DISTAL ENTERECTOMY ON GASTRIC SECRETION 

2. EFFECTS OF MASSIVE ENTERECTOMY AND AN AI'JTIPERISTALTIC SEGMENT ON 

GASTRIC SECRETION 




ADRIAN HOBART 


A THESIS 

SUBMITTED TO THE FACULTY OF GRADUATE STUDIES 
IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE DEGREE 

OF MASTER OF SCIENCE 


DEPARTMENT OF SURGERY 


EDMONTON, ALBERTA 


SPRING, 1970 


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FACULTY OF GRADUATE STUDIES 


The undersigned certify that they have read, and recommend 
to the Faculty of Graduate Studies for acceptance, a thesis entitled 
"1. Effects of Proximal Versus Distal Enterectomy on Gastric Secretion 
2. Effects of Massive Enterectomy and an Antiperistaltic Segment on 
Gastric Secretion" submitted by Adrian Hobart, in partial fulfilment 
of the requirements for the degree of Master of Science (Surgery). 


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ABSTRACT I 

Massive enterectomy is followed by gastric hypersecretion. 

The mechanism for this phenomenon is not known, although evidence sug¬ 
gests that it may be hormonally mediated. The effects of proximal and 
distal enterectomy on Heidenhain Pouch secretion in dogs, and the 
effects of thoracic duct lymph diversion and thoracic duct lymph re¬ 
infusion on these enterectomized dogs were studied. 

Baseline Heidenhain Pouch secretory studies were made under 
av/ake and anaesthetized, fed and fasting conditions, on twelve dogs. 

Six then had a 55% proximal enterectomy (Group A), and six a 55% distal 
enterectomy (Group B). In all dogs the stomach and duodenum were left 
intact. In the twenty-four hour collections, both groups showed a 
Heidenhain Pouch hypersecretion. In the eight hour studies. Group A 
dogs hyposecreted, while Group B maintained their hypersecretion. By 
contrast, when the diverted thoracic duct lymph was reinfused, the dogs 
of Group A hypersecreted, while the Heidenhain Pouch secretions of 
Group B remained unchanged. 

Our findings have demonstrated an unsuspected difference in 
Heidenhain Pouch secretion between proximal and distal enterectomies. 
Our results have shov;n a distal resection to be more effective than a 
proximal one in producing gastric hypersecretion. The thoracic duct 
lymph diversionary studies offer evidence of a secretogogue; the 




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decreased Heidenhain Pouch secrebion in Group A dogs suggests an ileal 
inhibitor to gastric secretion. Possible explanations, and clinical 
implications of these phenomena are discussed. 




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ABSTRACT II 

Death from cachexia within ninety days follows resection of 
80% of the small intestine in the dog. In the present study, 90% of 
the small intestine was resected in six dogs, and the subsequent 
deterioration allowed to proceed for approximately half the expected 
survival time. At this time, an 8 cm. length of proximal jejunum was 
reversed to act as an antiperistaltic segment. Ninety days after this 
procedure, the dogs were alive and healthy; the steep fall in body 
weight that followed massive enterectomy had been arrested, and the 
mean body weight had stabilized at 75% of the control figure. Barium 
x-ray studies demonstrated a delay in gastric emptying time after 
insertion of the antiperistaltic segment. The control time of four 
and one-half hours rose to six hours after segmental reversal. 

Although the therapeutic application of this experiment is 
clear, one of the undesirable sequelae of the operation was an increase 
in gastric secretion of up to 372% of the control value. The possible 
reasons for these findings are discussed. 


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ACKNOWLEDGEMENTS 

The completion of this work depends on the expert help of 
people from various disciplines, and this has been generously given 
during the preparation of this thesis. In particular, the author'is 
honoured to have received the skilled assistance of; 

Doctor W. W. Yakimets; whose continuing encouragement and proficiency 
as Supervisor were always able to reduce the problem to a 
manageable size. 

Doctor G. F. Bondar: whose vision enabled the pitfalls to be avoided, 
!4r. Ted Germaine and his Staff: whose day to day running of the 

operating room arrangements were designed to meet the needs 
of the individual. 

Mr. Serjio Ovejero: whose tireless technical assistance through a 

hundred operations, and v/hose diligent day to day care of the 
dogs throughout the year, (exemplified by naming them) were 
always cheerfully and most conscientiously given. 

Mr. John Henriksen: whose talent and experience with the dogs were 
instrumental in producing clear barium x-ray studies, 

Mr. Ralph McNabb, and my wife, Jo; whose art work was tastefully and 
expeditiously executed despite heavy commitments. 

The Staff of the University Hospital Photographic Department, whose 

cordiality and speed in making numerous prints were exemplary. 


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Mrs, June Dowson, of the John Scott Library, and Miss Phyllis Russell 
and her Staff at the Cameron Library; v/hose enthusiasm and 
expertise at finding needles in haystacks was a source of 
continuing help and encouragement. 

Professor Ursula von Maydell, Mr. Mike Grohn and Mr, Dave Lougheed; 

whose organization of the statistical analyses were meticulously 
programmed and performed on the University Computer, 

Mrs, Arlene Lyon; who painstakingly typed the manuscript. 

The Edmonton Civic Employees Welfare Chest Fund, whose generosity made 
this research financially possible, 




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TABLE OF CONTENTS 

PART 1. EFFECTS OF PROXIMAL VERSUS DISTAL ENTERECTOMY 

ON GASTRIC SECRETION 

PAGE 

REVIEW OF PHYSIOLOGICAL REGULATION OF GASTRIC SECRETION ..... 1 

I. Vagal Mechanism .. ... ,2 

II. Antral Mechanism 6 

III. Intestinal Mechanism .. in 

IV. Miscellaneous . , . .. 17 

Visceral . 17 

Local Factors 19 

Work Challenge 20 

V, Conclusion , 21 

METHODOLOGY.... , 32 

I. General . 32 

II. Experimental Plan 32 

III. Before Operation . 33 

IV. Operation ..... 34 

V. Heidenhain Pouch Construction 34 

VI, Proximal Enterectomy , . 36 

VII . Distal Enterectomy 38 

VIII. Thoracic Duct Cannulation 38 

IX. Postoperative Management 40 

X. Collection of Samples 41 





















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XI. Determination of Gastric Acidity, . , . 

RESULTS ..... . 

I. First Stage . 

Twenty-Four Hour Measurements . 

Eight Hour Awake Measurements . 

Eight Hours Awake Fed Secretions 

Eight Hours Awake Fasting Secretions ....... 

Eight Hour Anaesthetized Measurements ........ 

Eight Hours Anaesthetized Fed Secretions , . . . . 
Eight Hours Anaesthetized Fasting Secretions . . . 

II. Second Stage 

Group A ... 

Group B , 

General ^ . 


DISCUSSION 




I. Tv/enty-Four Hour Studies . 

II, Eight Hour Studies 

III. Possible Mechanisms of Gastric Hypersecretion Following 

Enterectomy , 

Potentiation of Secretogogues , 

Prolonged Gastric Emptying Time 

Liver Damage . 

Infectron. . . . . . . . , . . . . . . . , . . . . 







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PAGE 

Intestinal Phase . . 98 

Removal of Inhibitors .. 99 

IV. Conclusions .. 104 

PART 2. EFFECTS OF .MASSIVE ENTERECTOMY AND AN ANTIPERISTALTIC SEGMENT 

ON GASTRIC SECRETION 

REVIEW OF THE LITERATURE ON REVERSED INTESTINAL SEGMENTS . . , , 109 

METHODOLOGY ..... . ............ 118 

I. General . . .................. 118 

II. Experimental Plan ................... 118 

III. Before Operation , 119 

IV. Operation .. ........... . 119 

V. Heidenhain Pouch Construction ............. 120 

VI. Enterectomy ...................... 120 

VII. Segmental Reversal .................. 123 

VIII. Postoperative Management ............... 125 

IX. Collection of Samples ................. 126 

X. Laboratory Procedures ................. 127 

Determination of Gastric Acidity 127 

RESULTS . , . ........ 129 

I. Twenty-Four Hour Heidenhain Pouch Secretions ..... 129 

Control ..... . ........... 129 

After Massive Enterectomy 129 

After Segmental Reversal. 133 

II. Eight Hour Awake Heidenhain Pouch Secretions ..... 133 























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Control . 133 

After Massive Enterectoniy . . , . .. 134 

After Segmental Reversal . I34 

III, Eight Hour Anaesthetized Heidenhain Pouch Secretions. . 138 

Control. 138 

After Massive Enterectomy ... , , . , 138 

After Segmental Reversal .. 138 

IV. Body Weights 142 

V. Gastric Emptying Times 142 

Controls . 142 

After Massive Enterectomy . 145 

After Segmental Reversal . . 145 

DISCUSSION.. , .. 156 

I. Increase in Gastric Secretion ...... . 156 

II. Increase in Transit Time , . 157 

III. Decline in Body Weight. . 159 

BIBLIOGRAPHY.,... 164 



















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LIST OF TABLES 


PART 1. EFFECTS OF PROXIMAL VERSUS DISTAL ENTERECTOMY 

ON GASTRIC SECRETION 


TABLE PAGE 

1. Mean Total Postprandial Heidenhain Pouch Secretions in 

Control Dogs, Dogs with 55% Proximal Enterectomy 
(Group A), and Dogs with 55% Distal Enterectomy 
(Group B). Volumes, Free Acid and Total Acid Con- 
centrations are Shown, and the Statistical Significance 
of the Changes Follov/ing Enterectomy 47 

2. Mean Total Fasting Heidenhain Pouch Secretions in Control 

Dogs, Dogs with 55% Proximal Enterectomy (Group A), and 
Dogs with 55% Distal Enterectomy (Group B). Volumes, 

Free Acid and Total Acid Concentrations are Shov/n, and 
the Statistical Significance of the Changes Following 
Enterectomy .... . 49 

3. Mean Total Eight Hourly Heidenhain Pouch Secretion in Av/ake 

Controls and Enterectomized Dogs, Fed and Fasting, and the 


Statistical Significance of the Changes Following 

Enterectomy 56 

4. Mean Hourly Heidenhain Pouch Secretions in Awake Dogs ... 57 

5. Mean Hourly Heidenhain Pouch Secretions in Awake Dogs 

Group A (Proximal Enterectomy) , . 58 

6 . Mean Hourly Heidenhain Pouch Secretions in Awake Dogs 

Group B (Distal Enterectomy) 59 


7. Mean Total Eight Hourly Heidenhain Pouch Secretions in 
Anaesthetized Controls and Enterectomized Dogs, Post¬ 
prandial and Fasting, and the Statistical Significance 


of the Changes Following Enterectomy 65 

8 . Mean Hourly Heidenhain Pouch Secretions in Anaesthetized 

Dogs Controls 66 


9. Mean Hourly Heidenhain Pouch Secretions in Anaesthetized 
Dogs Group A (Proximal Enterectomy) 








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xill 


TABLE 


PAGE 


10. Mean Hourly Heidenhain Pouch Secretions in Anaesthetized 

Dogs Group B (Distal Enterectomy) 

11. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures ^ 

12. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 

Collection with Control Figures ............... 

13. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 

14. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection V7ith Control Figures 


68 


77 


78 


79 


80 


15. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 

16. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 


17. Statistical Analysis Comparing Mean Heidenhain Pouch 
Secretions Under the Various Conditions of 
Collection with Control Figures 


18. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures .... . 

19. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures ......... 


20. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures .......... 

21. Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 

22. Statistical Analysis Comparing Mean Heidenhain Pouch 

ggcretions Under the Various Conditions of 
Collection with Control Figures ......... 





















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XIV 


TABLE 

23, Hourly Heidenhain Pouch Secretion in Group A Dogs During 

Baseline Collections (Hours One and Two), Postprandial 
Collections with Thoracic Duct Lymph Diverted (Hours 
Three, Four, Five and Six) , and Post Lymph. Rein-- 
fusion Collections (Hours Seven and Eight); and Mean 
Hourly Volumes and Acid Concentrations ......... 

24, Individual Hourly Heidenhain Pouch Secretion in Group B 

Dogs During Baseline Collections (Hours One and Two), 
Postprandial Collections with Thoracic Duct Lymph 
Diverted (Hours Three, Four, Five, and Six), and Post 
Lymph, Reinfusion Collections (Hours Seven and Eight); 
and Mean Hourly Volumes and Acid Concentrations . , , . 

25, Comparison of Hours Seven and Eight with the First Six 

Hours of Secretion in the Thoracic Duct Diversion in 
Proximal Enterectoray . , . 

26, Comparison of Hours Seven and Eight with the First Six 

Hours of Secretion in the Thoracic Duct Diversion in 
Distal Enterectomy 

27, Mean of the First Six Hours of the Thoracic Duct Diversion 

in Dogs with Distal Enterectomy Compared with the Mean 
of the First Six Hours of Duct Diversion in Dogs with 
Proximal Enterectomy 

28, Mean of the Last Two Hours of the Thoracic Duct Diversion 

in Dogs with Distal Enterectomy Compared to the Last 
Two Hours of the Proximal Duct Diversion 


PAGE 


89 


90 


91 


92 


93 


94 


PART 2. EFFECTS OF J4ASSIVE ENTERECTOMY AND AN ANTIPERISTALTIC SEGMENT 

ON GASTRIC SECRETION 

1. Mean Total Twenty-Four Hour Awake Postprandial Heidenhain 
Pouch Secretory Volumes, Free and Total Acid Concentra¬ 
tions, in Control Dogs, Enterectomized Dogs (Group A), 
and Dogs with an Antiperistaltic Jejunal Segment (Group 
B), Statistically Significant Increases (p = 0.01) were 
Noted in Heidenhain Pouch Secretory Volme, Free and 
Total Acid Concentrations, After Both Operative Procedures . 131 







-4 

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XV 


TABLE 

2. Mean Total Twenty-Four Hour Awake Fasting Heidenhain Pouch 

Secretory Volumes, Free and Total Acid Concentrations, in 
Control Dogs, Enterectomized Dogs (Group A), and Dogs 
with an Antiperistaltic Jejunal Segment. No Statistically 
Significant Change Following Enterectomy, but after In¬ 
sertion of the Reversed Segment, Significant Changes were 
Noted in Heidenhain Pouch Secretory Volume, Free and Total 
Acid Concentrations .................... 

3. Mean Total Eight Hour Awake Postprandial Heidenhain Pouch 

Secretory Volumes, Free and Total Acid Concentrations, 
in Control Dogs, Enterectomized Dogs (Group A) and Dogs 
with an Antiperistaltic Jejunal Segment (Group B), 

None of the Heidenhain Pouch Secretory Changes Following 
Either Procedure was Statistically Significant 

4. Mean Total Eight Hour Awake Fasting Heidenhain Pouch 

Secretory Volumes, Free and Total Acid Concentrations, 
in Control Dogs, Enterectomized Dogs (Group A ), and 
Dogs with an Antiperistaltic Jejunal Segment (Group B), 

No Statistically Significant Secretory Change was 
Observed After Either Procedure 

5. Mean Total Eight Hour Anaesthetized Postprandial Heidenhain 

Pouch Secretory Volumes, Free and Total Acid Concentra¬ 
tions, in Control Dogs, Enterectomized Dogs (Group A), 
and Dogs with an Antiperistaltic Jejunal Segment (Group 
B). None of the Secretory Changes Following Either 
Procedure was Statistically Significant 

6 . Mean Total Eight Hour Anaesthetized Fasting Heidenhain 

Pouch Secretory Volumes, Free and Total Acid Concentra¬ 
tions, in Control Dogs, Enterectomized Dogs (Group A), 
and Dogs v;ith an Antiperistaltic Jejunal Segment (Group 
B). None of the Secretory Changes Following Either 
Procedure was Found to be Statistically Significant . , . , 

1^ Statistical Analysis of the Changes in Twenty-Four Hour 
Total Av/ake Postprandial Heidenhain Pouch Secretory 
Volumes, Free and Total Acid Concentrations, in Control 
Dogs (El), Enterectomized Dogs (E2) and Dogs with an 
Antiperistaltic Jejunal Segment (E3)............ 


PAGE 


132 


136 


137 


140 


141 


150 









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XVI 


TABLE PAGE 

s 

2 Statistical Analysis of the Changes in Twenty-Four Hour 

Total Awake Fasting Heidenhain Pouch Secretory Volumes, 

Free and Total Acid Concentrations in Control Dogs (El), 
Enterectomized Dogs (E2), and Dogs with an Anti- 

peristaltic Jejunal Segment (E3} 151 

s 

3 Statistical Analysis of the Changes in Eight Hour, Hourly 

Awake Postprandial Heidenhain Pouch Secretory Volumes, 

Free and Total Acid Concentrations, in Control Dogs (El), 
Enterectomized Dogs (E2) and Dogs with an Anti- 

peristaltic Jejunal Segment CE3) 152 

3 

4 Statistical Analysis of the Changes in Eight Hour, Hourly Awake 

Fasting Heidenhain Pouch Secretory Volimies, Free and Total 
Acid Concentrations, in Control Dogs CEl), Enterectomized 
Dogs (E2) and Dogs with an Antiperistaltic Jejunal Segment 

CE3) ..... 

rS . . , . 

5 Statistical Analysis of the Changes in Eight Hour Anaes¬ 

thetized Postprandial Heidenhain Pouch Secretory Volumes, 

Free and Total Acid Concentrations, in Control Dogs (El), 
Enterectomized Dogs (E2) and Dogs with an Antiperistaltic 
Jejunal Segment (E3) . 

3 

6 Statistical Analysis of the Changes in Eight Hour, Hourly 

Anaesthetized Fasting Heidenhain Pouch Secretory Volumes, 

Free and Total Acid Concentrations, in Control Dogs (El), 
Enterectomized Dogs (E2), and Dogs with an Anti¬ 
peristaltic Jejunal Segment (E3) 


153 


154 


155 






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XVll 


LIST OF ILLUSTRATIONS 


PART 1. EFFECTS OF PROXHIAL VERSUS DISTAL ENTERECTOMY 

ON GASTRIC SECRETION 


FIGURE PAGE 

1. Heidenhain Pouch ...... . 35 

2. 55% Proximal Enterectomy . , 37 

3. 55% Distal Enterectomy , . , ... , . . . 39 

4. Comparison of the Mean Twenty-Four Hour Postprandial 

Heidenhain Pouch Secretion in Control Dogs, and 
Enterectomized Group A and Group B Dogs. Secretion 
was Significantly Increased in both Groups (p = 0.05). 

Free and Total Acid was Significantly Increased 

(p = 0,05) in Group A Dogs, but not in Group B Dogs. .... 46 

5. Comparison of the Mean Twenty-Four Hour Fasting Heidenhain 

Pouch Secretion in Control Dogs, and Enterectomized Group 
A and Group B Dogs. Secretion was Increased in Group A, 
and the Free and Total Acid was Increased in both Groups. 

None of these Increments was Statistically Significant ... 50 

6 . Comparison of the Mean Hourly Awake Postprandial Heidenhain 

Pouch Secretory Volumes of Control Group, Group A and Group 
B Dogs. Post Enterectomy, the Volume of Group A Secretions 
Diminished, and that of Group B Increased. Neither Change 
was Statistically Significant . . 51 

7. Comparison of the Mean Hourly Awake Postprandial Heidenhain 

Pouch Acid Concentrations of Control Dogs, Group A and 
Group B Dogs. Post Enterectomy, the Acid Level of Group A 
Diminished, and that of Group B Increased. Neither Change 
was Statistically Significant. .... . ... 

8 . Comparison of the Mean Hourly Awake Fasting Heidenhain Pouch 

Secretory Lumes of Control Group, Group A and Group B Dogs, 

Post Enterectomy, the Secretory Lxmies of Both Groups 
Decreased Significantly (p = 0.05) 


54 









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XVlll 


FIGURE 

9, Comparison of the Mean Hourly Awake Heidenhain Pouch Acid 
Concentrations in Awake and Fasting Control Dogs, Group 
A and Group B Dogs, Post Enterectomy, in Group A There 
was a Significant Decrease in the Free Acid (p = 0.01) 
and the Total Acid (p = 0.01) and in Group B a Signifi¬ 
cant Decrease in the Free Acid (p = 0.01) and the Total 
Acid (p = 0.05) . 

10. Comparison of the Mean Hourly Anaesthetized Postprandial 

Heidenhain Pouch Secretory Volumes of Control Dogs, 

Group A and Group B Dogs. Enterectomy had no Signifi¬ 
cant Effect on that of Group A, but Significantly In¬ 
creased that of Group B Cp = 0.05), 

11. Comparison of the Mean Hourly Anaesthetized Postprandial 

Heidenhain Pouch Acid Concentrations of Control Dogs, 

Group A and Group B Dogs. Enterectomy Significantly 
Decreased the Free and Total Acid Concentration in 
Group A (p = 0.05), and Significantly Increased the 
Free and Total Acid in Group B Cp - 0,05) ... 


PAGE 


55 


61 


62 


12. Comparison of the Mean Hourly Anaesthetized Fasting 

Heidenhain Pouch Secretory Volimes of Control Dogs, 

Group A and Group B Dogs, No Significant Changes 

Occurred Following Enterectomy 63 

13. Comparison of the Mean Hourly Anaesthetized Fasting 

Heidenhain Pouch Acid Concentrations of Control Dogs, 

Group A, and Group B Dogs, Enterectomy Produced a 

Significant Fall in Free and Total Acid Concentration 

in Group A (p = 0.05) but no Significant Change in 

Group B Dogs.. . . ... 64 


14, Comparison of the Mean Hourly Heidenhain Pouch Secretory 

Volumes of Anaesthetized and Thoracotomized Group A and 
B Dogs. Feeding and Diversion of the Thoracic Duct 
Lymph had no Measurable Effect on Either Group, Rein¬ 
fusion of Diverted Lymph Significantly Increased the 
Secretory Volume (p = 0.01) of Group A Dogs, but had 
no Significant Effect on that of Group B Dogs 71 

15, Comparison of the Mean Hourly Heidenhain Pouch Acid Con¬ 

centrations in Anaesthetized and Thoracotomized Group 
A and B Dogs. Feeding and Diversion of Thoracic Duct 
Lymph had no Measurable Effect in Either Group, Rein¬ 
fusion of Diverted Lymph Significantly Increased the 
Free and Total Acid Concentration (p = 0,01) in Group 
A, but had no Significant Effect in Group B . 


72 








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XIX 


FIGURE PAGE 

16, Hourly Heidenhain Pouch Secretory Volumes in Anaesthetized 

and Thoracotomized Group A Dogs, Mean Volumes for the 

Two Hour Fasting, Four Hour Postprandial Lymph Diverted, 

and Two Hour Lymph Reinfusion Periods are Illustrated 

with a Dotted Line .. 73 

17, Hourly Heidenhain Pouch Secretory Volumes in Anaesthetized 

and Thoracotomized Group B Dogs, Mean Volumes for the 

Two Hour Fasting, Four Hour Postprandial Lymph Diverted 

and Two Hour Lymph Reinfusion Periods are Illustrated 

with a Dotted Line 74 

18, Comparison of Mean Heidenhain Pouch Secretory Volumes in 

Anaesthetized and Thoracotomized Group A and B Dogs for 

the Two Hour Fasting, Four Hour Postprandial Lymph 

Diverted, and Two Hour Lymph Reinfusion Periods 76 

PART 2. EFFECTS OF MASSIVE ENTERECTOMY AND AN ANTIPERISTALTIC SEGMENT 

ON GASTRIC SECRETION 


1. Heidenhain Pouch . 121 

2, Massive Enterectomy . 122 


3. Insertion of an 8 cm. Antiperistaltic Segment 124 

4. Effect of Enterectomy and Subsequent Insertion of an Anti¬ 

peristaltic Segment, on Mean Total Twenty-Four Hour Post¬ 
prandial and Fasting Secretion. Both Enterectomy and 
Reversal Significantly Increased Heidenhain Pouch Secre¬ 
tion in Postprandial Dogs (p = 0.01) as Compared to the 
Controls, There was no Significant Increase in Heidenhain 
Pouch Secretion after Enterectomy in Fasting Dogs, but 
Reversal Resulted in a Significant Increase (p = 0.05). . . 130 

5. Effect of Enterectomy and Subsequent Insertion of an Anti¬ 

peristaltic Segment on Mean Total Eight Hour Heidenhain 

Pouch Secretory Volumes in Awake Dogs. No Significant 

Changes were Observed after Either Procedure as Compared 

to the Controls ... . , .. 135 

6 . Effect of Enterectomy and Subsequent Insertion of an Anti¬ 

peristaltic Segment on Mean Total Eight Hour Heidenhain 
Pouch Secretory Volumes in Anaesthetized Dogs, No 
Statistically Significant Changes were Observed after 
Either Procedure 


139 











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XX 


FIGURE 

7. Comparison of the Mean Body Weights of Dogs Before 

Enterectomy, Two Months after Massive Enterectomy^ 

and Two and Three Months after Reversal of a 

Jejunal Segment . , . 

8 . Bariimi X-rays of Control Dog's (13591 Gastric Emptying 

Time. The Plate on the Left Shows the Stomach a Few 
Minutes after the Dog had Swallowed the Barium Mixture. 
The Plate on the Right Shows the Same Stomach Empty 
Three Hours Later . .... 

9. - Bariiam X-rays of Dog 1359 after Enterectomy. The Plate 

on the Left Shows the Stomach a Few Minutes After the 
Dog had Swallowed the Bariiom xMixture. The Plate on 
the Right Shows the Same Stomach Empty Three Hours 
Later ...... 

10, Barium X-rays of Dog 1359 after Insertion of an Anti- 

peristaltic Segment. The Plate on the Left Shows the 
Stomach a Few Minutes after the Dog had Swallowed the 
Barium Mixture. The Plate on the Right Shows the 
Same Stomach Remaining Partially Full Three Hours 
Later.. , 

11, Barium X-ray of Dog 1359 after Insertion of an Anti- 

peristaltic Segment. The Stomach is Almost Empty of 
the Barium Mixture at Six Hours after its Ingestion, 
Demonstrating a Long Delay in Gastric Emptying After 
Segmental Reversal . , . , . 


PAGE 


143 


144 


146 


147 


148 









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PART 1, EFFECTS OF PROXIMAL VERSUS DISTAL ENTERECTOMY 


ON GASTRIC SECRETION 




REVIEW OF PHYSIOLOGICAL REGULATION 
OF GASTRIC SECRETION 

Modern scientific study of gastric physiology begins with 
observations of secretions made on patients with gastric fistulae. In 
1824, Doctor Beaumont (1) stopped trying to heal the wound in the 
abdomen of Alexis St. Martin, and concentrated on recording the intra- 
gastric happenings such as the change of color and contour with mood. 
Shortly after this, Bassov and Blondlot (2) described the production 
of gastric fistulae in dogs for experimental purposes, and from this 
time onwards, the detailed study of the working of the living stomach 
was no longer dependent upon fortuitous accidents. A. J. Carlson (3) 
reported on three such human patients in the nineteen twenties from 
his Chicago laboratory, and towards the end of World War II, Wolf and 
Wolffe (4) made extensive studies on the fistula of Tom Little. 

At the turn of the century, the studies of Pavlov (5) began to 
indicate the complexity of the control of gastric secretion. The canine 
stomach was used as an experimental model from which various pouches 
could be fashioned, and a rapid accumulation of basic knowledge of its 
working began to take place. It is instructive to trace the chrono¬ 
logical development of the discoveries in the three main mechanisms 
that are now thought to affect gastric secretion—vagal, antral and 
intestinal. This is not only the order in which they were discovered, 


1 


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but also the order of their relative importance of their contribution 
to gastric secretion. 

I. Vagal Mechanism 

Beaun-iont had been surprised to find that gastric juice would 
flow at the anticipation of food, just as emotions like anger or dis¬ 
gust would halt the flow. Other workers, such as Richet, (1878) (6), 

noted that the actual consumption of food was not necessary to produce 
a gastric secretion, but it was not until the turn of the century that 
Pavlov provided the explanation. He demonstrated the importance of the 
vagus nerves in mediating gastric secretion in his classical experiment 
with dogs in 1895. 

From their laboratory, Ivan Pavlov and Mme, Schumann- 
Simionovskaja showed that gastric secretion was not solely a function of 
the digestive tract. They built up a conditioned reflex in the dog, 
in which the feeding was accompanied by the ringing of a bell during 
the period of reinforcement. Subsequent presentation only of the 
neutral stimulus was able to evoke the digestive response for a time, 
and it was this phenomenon that led Pavlov to give up his work on the 
digestive glands, and concentrate his efforts on the nervous system. 
Implicating the vagus nerve as the logical anatomical link between 
the two organs, he cut the oesophagus in the neck, and brought the two 
ends out as separate openings. Gastric juice would flow when the 
animal was'"sham fed" through the mouth, even though the food would 
leave the oesophagus in the upper neck. The flow of gastric juice was 
often prolonged and copious, but was abolished when the vagi were 



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interrupted, demonstrating this to be the efferent pathway. 

Changes in the colour and motility of the gastric mucosa 
under different psychical conditions have been subsequently recorded 
through the years by many workers, namely Carlson (1923), Uvnas (1942) 
(7), Wolf and Wolff (1943), and many others. 

Experiments on patients under hypnosis, by Bennett and 
Venables in 1920 (8), gave rise to secretion of gastric juice at the 
suggestion of enjoyable food, and to inhibition of the flow at the 
mention of disgusting substances. Other investigators have demon¬ 
strated an impaired flow of gastric juice when food is served in an 
unappetizing manner. 

The role of the vagus nerve in the release of gastrin has been 
extensively studied by Grossman (9). He reports that cholinergic 
reflexes mediate the release of gastrin in both the "cephalic" and 
"gastric" phase of gastric secretion. In the cephalic phase, reflexes 
are mediated solely by the vagi, and are of two kinds; (a) direct 
cholinergic stimulation of parietal cells, (b) cholinergic release 
of gastrin from pyloric gland cells. In the gastric phase, he claims 
that the same mechanisms occur, but are mediated both by the vagi and 
local intramural pathways. Evidence for the latter is furnished by 
Bedford (10) , who shov/ed in 1962 that topical anaesthetics applied to 
the gastric mucosa prevented the gastrin release formerly provoked by 
local stimuli. 

As the complex concept of the control of gastric secretion 
gradually becomes clearer, the notion of separate "phases" acting in 


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unison is losing ground, and being replaced by the idea of different 
mechanisms acting in harmony (11). There is an interweaving of 
secreting agents, and an interdependence of their machinery. Never™ 
theless, since it is technically feasible to ablate the action of the 
vagus nerve in toto, it is instructive to observe the changes in 
secretion both with and without this neurogenic influence. Bilateral 
truncal vagotomy results in a decreased secretion of gastric acid, and 
decreased gastric motility C121, But the inhibition of gastric juice 
produced by the presence of fat in the duodenum is unaffected by 
vagotomy. On the other hand, the response to endogenous gastrin in a 
vagally innervated pouch is reduced by about fifty per cent once this 
innervation is ablated, (Dragstedt, 1966), (13). The traditional 
response to gastrin and to Histamine has been shown to drop by about 
thirty per cent in vagotomized cats (Emas and Grossman, 1967), (14). 

French (151 reported in 1953 that electrical stimulation of 
the anterior hypothalamus produces an increase in gastric secretion, 

This result was preventable by vagotomy, but not by adrenalectomy. 

Next, stimulation of the posterior hypothalamus resulted in delayed 
secretion; and this was prevented by adrenalectomy, but not by 
vagotomy. The first part of this experiment was repeated by Mason in 
1967 (16), with similar results. 

The error of considering the vagal contribution to be ex™ 
clusively inhibitory or stimulatory is shown by the experiments of 
Dragstedt, Johnson, Singer^ and Oberhelman in 1960 (17). Although trun™ 
cal vagotomy was now accepted as a procedure for reducing gastric acid 


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secretion, these workers confirmed the findings of Storer et al (1952) 

(18) that cutting the vagi to the main stomach caused an increased 
Heidenhain Pouch acid output, and that vagotomy of the small intestine 
produced a smaller rise in Heidenhain Pouch secretion. The proposed 
explanation for these phenomena is the secondary stimulation of antral 
gastrin, or a gastrin potentiator, thus increasing the contribution of 
the hormonal phase. 

Another example of vagally-stimulated gastrin release is seen 
in the gastric hypersecretion following insulin-induced hypoglycaemia. 
This hypersecretion is initiated by degrees of hypoglycaemia of about 
half the normal blood sugar level (e.g. about 40 mgm. %), while lesser 
degrees produce a mild inhibition of gastric secretion. Nyhus et al 

(19) have demonstrated a thirty-fold increase in free HCl in dogs two 
hours after the intravenous administration of ten units of insulin. 
Grossman (20) , hov/ever, had shown a twenty-fold increase in free HCl 
in antrectomized and enterectomized dogs an hour after insulin admini¬ 
stration. The former finding is probably an example of vagal release 
of gastrin since his extrinsically innervated antra were isolated from 
acid and from local mechanical and chemical stimuli, and yet produced 
a significant acid secretory response following vagal stimulation. 

After denervation by antroneurolysis, acid production by insulin-induced 
vagal stimulation ceased. The latter finding is a direct effect on the 
parietal cells of hypothalamic stimulation of the vagus nerve, since 
all the known sites of gastrin production have been extirpated. Gross- 
man (20) also found that intra-arterial infusion of acelylcholine pro- 



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duced an acid secretory response in the fundus, after all known sites 
of gastrin production had been removed, inferring from this that the 
main mechanism of stimulation of acid secretion by vagal stimulation 
is a direct cholinergic action on the fundic glands, demonstrating 
again the overall complexity of the different agents at work, and the 
fallibility of regarding the mechanisms as separate entities. 

II. Antral Mechanism 

One of the earliest observations made in connection with 
gastric physiology was that food in the stomach caused a rise in the 
secretion of gastric juice. Pavlov had demonstrated this both in 
waking and narcotized subjects. In 1906, Edkins (21) made an extract 
of antral mucosa which, when injected intravenously into dogs, pro¬ 
duced a brisk rise in gastric secretion. Pavlov had shown that acid 
introduced into the duodenum acted as an inhibitor of gastric juice, 
and in 1910, Bayliss and Starling (22) demonstrated the same result 
by instilling acid into the pyloric antrum. There is no general agree 
ment as to the mechanism by which these inhibitions are produced, but 
evidence exists that humoral mediation is responsible in the case of 
the duodenum, since duodenal acidification reduces secretion from 
vagally-denervated fundic pouches (23). Nerve reflexes involving the 
vagus have been implicated by Sircus (24) in reducing gastric secre¬ 
tion after duodenal acidification. The inhibition of gastric acid 
secretion produced by antral acidification had been thought to be 
the result of local action of the lowered pH on the antral mucosa, or 






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an indirect action via the vagal nerve to the stomach. In 1956, 
Harrison, Lakey and Hyde (25) proposed another mechanism—an antral 
inhibitory hormone. Like the intestine, the antrum was now known to 
be able to stimulate or inhibit the flow of gastric juices. 

In 1920 Popielski (26), working with Edkin's extract, con¬ 
cluded that it was Histamine, demonstrating for later workers the 
actions of this drug on gastric secretion. His conclusion was based 
on this extract's powerful stimulation of gastric secretion, and for 
many years its true nature v/as in doubt. But it gradually became clear 
that Histamine, apart from having systemic side effects of constricting 
smooth muscle and producing bronchospasm, was less potent than Edkin's 
substance in stimulating the flow of gastric juice, and subsequent 
refinements of technique showed that although Histamine was usually 
present in these tissue extracts, the substance under discussion was 
not inactivated by Histaminase. It was found to be a true hormone, 
and was named gastrin by Edkins. Attention was now focused on the 
antrum as the source of this stimulator, and in 1925, Lim and McCarthy 
(27) removed the fundus of the stomach and performed a vagotomy in a 
series of dogs, leaving only the antrum in alimentary continuity. 

When these dogs were fed, there was a rise in gastric secretion. Food 
in the antrum was thus shown to be the normal stimulus for gastrin 
production, although subsequently a wide variety of different substances 
was seen to be effective in promoting a flow, including simple dis¬ 
tension with a balloon. Duval and Price (28) reproduced this remark¬ 
able finding with the subject anaesthetized, but later Lim and Mozer 


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8 

(29) were able to abolish it when the antrum was locally anaesthetized, 
suggesting the possible existence of a mechanical as well as a chemical 
pathway. 

Further advances in this field came from the v/ork of Gregory 
and Ivy (30). In 1941, they made separate transplants of antrum and 
fundic pouch, and were able to collect secretion from both when the 
dog was fed, thus establishing the criteria for a hormonal mechanism. 
Later in the year, they devised experiments which demonstrated that 
the release of gastrin is dependent on cholinergic nerve-endings in 
the antral mucosa. 

The exact confines of the antrum have been ingeniously 
delineated in vivo by Bergstrom and Broom in Sweden, in 1964 (31) by 
the change in colour of pulverized litmus sxjrayed over the gastric 
mucosa following a systemic Histamine challenge. In view of the con¬ 
siderable individual variation in the boundary between fundus and 
antrum, this method is better tailored to the requirements of the in¬ 
dividual than the suggestion made in 1963 by Ruding and Hirdes (32) 
that at least eighty per cent of the lesser curve be resected in an 
antrectom.y, this being the limit of the antral tissue as determined 
histologically by them in thirteen stomachs. 

In 1951, Dragstedt (33) showed that the inhibition of gastric 
secretion by acid in the stomach was contingent on contact between the 
acid and cells of the pyloric mucosa, and implied a local mechanism at 
the cellular level, mediated by pH. In 1960, some of the data produced 
in a cross-circulation experiment by Duval and Price (34) made it clear 





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that acid introduced into the antrum on one dog would depress the 
antral secretion of another dog with whom it is cross-circulating, 
the latter dog's antrum having previously been stimulated to secrete 
by gentle inflation of a previously placed antral balloon with 15-25 
ml, of air. The following year, Thompson and Lerner, (35) in another 
cross-circulation experiment, confirmed this finding when, after 
irrigating one antrum with acid, they were able to diminish the 
secretion in another denervated Heidenhain Pouch, 

Recent work has shown that gastrin has many actions, and these 
have been classified, for experimental purposes, into (a) those re¬ 
producible by small doses of exogenous gastrin, and (b) those repro¬ 
ducible by large intravenous doses of exogenous gastrin, these latter 
effects not being produced at all by endogenously released gastrin. 

One paradoxical and so far unexplained finding in this regard was that 
of Gillespie and Grossman in 1963 (36), who discovered that a very 
large dose of exogenous gastrin actually inhibited gastric secretion. 
Evidence was furnished in 1963 by Menguy (37) that canine antral mucus 
has a high concentration of gastric inhibitory substance, and that 
this concentration is increased by vagal denervation of the antrum, 

Fundic secretion v/as not found to have any inhibitory action, and 
canine saliva was found to be weakly inhibitory. In a recent assay 
(1967) (38) , a pure foinn of gastrin (probably the physiologically active 

constituent) was synthesized from hog antral mucosa. This was found to 
have approximately the same effect on gastric secretion as has Histamine, 
without having the unv/anted side effects of Histamine. 


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Schofield (39) has found that an alkaline pH in the pyloric 
antrum leads to an increased flow of gastric juice, as might be ex¬ 
pected from the foregoing studies with acid in the same site. In 
1965 he found that the acid response to meat extract in the antrum was 
abolished by the administration of Atropine, showing that cholinergic 
nerve endings in the antral mucosa are involved in the pathwav, and 
reinforcing the views of other workers that maximal gastric secretion 
is dependent on vagal and antral stimuli working together in concert, 
and is not forthcoming if the activity of one of these mechanisms is 
impaired, 

III. Intesti n al Mech anism 

From the simple and direct experiments with gastric fistulae, 
it was known that meat extracts, bread, egg white, meat, milk and 
liver introduced into the stomach caused a rise in gastric secretion. 

In 1900, Le Conte (40) demonstrated a similar phenomenon from' certain 
foods in the intestine, the mechanism of which remains incompletely 
explained today. At the same time Pavlov (41) was showing that the 
introduction of acid into the duodenum actually inhibited the flow of 
gastric juice, while Sokolov (42) was achieving the same result using 
gastric juice itself as the agent. The following year, Bayliss and 
Starling (43) , v/ith their isolation of secretin, showed that one of 
the actions of this hormone was to inhibit gastric secretion (while 
stimulating that of the pancreas). Secretin, they found, was liberated 
from the duodenal mucosa following the action of acid, fat, fatty acids, 



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amino acids or water on the stomach or intestine. 

The inhibitory effect of fat in the duodenum on both gastric 
secretion and motility was next recognized, and in 1926 this was 
demonstrated by Farrell and Ivy (44) to be independent of the nerve 
supply. On the basis of further experiments which suggested that this 
chalone was secreted from the wall of the proximal small intestine, 
this hormone was named "enterogastrone" by Kosaka and Lim in 1933 (45) . 
In 1928 a similar phenomenon was recorded by Ivy and Olberg, (46) when 
they noted a decrease in gastric secretion together with contraction 
of the gallbladder produced by a hormone which they called "cholecysto- 
kinin". This hormone was liberated as a result of contact with the 
upper intestinal mucosa of acid chyme, fats and their hydrolysates. 

Ivy claimed that cholecystokinin was formed and absorbed into the blood 
stream during intestinal digestion; but whether this hormone is suf¬ 
ficient to cause a physiologically significant depression of gastric 
secretion remains dubious, and the "search for a specific chalone in 
the duodenal mucosa must continue"--Sven Anderssen, 1967 (47). 

The next twenty years saw numerous substances investigated 
which, when placed in the intestine, gave rise to an increased gastric 
secretion. Babkin (48) showed that the introduction of peptone (and 
other products of protein digestion) into the small intestine stimulated 
gastric secretion. Later, Beamer, in 1944 (49) showed that the presence 
of bile was necessary in the upper intestine before peptone-like sub¬ 
stances in the same site would promote increased gastric secretion, 
and then only after a latent period of about two hours. Babkin also 






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showed that excessive administiration of Vitamin D depiressed gastiric 
secretion; further studies revealed that this was due to the corres¬ 
ponding increase in the blood calcium level, and that variations above 
or below the normal range will reproduce this inhibition. 

The isolation of Serotonin in 1952 (Erspamer and Asero) (50) 
provided a substance which would, inter alia, inhibit gastric secretion 
while stimulating gastrointestinal motility—Olsen and Gray (51); 

Black and Fisher, 1958 (52). While this was being done, Resnick (53) 
showed the occurrence of Serotonin in the duodenum and jejunum. 

In 1963, Silen, Hein, Albo and Harper (54) from the University 
of California published the results of their work with the biliary 
apparatus on gastric secretion. They found that obstruction of the 
common bile duct led to gastric hypersecretion, which persisted and 
increased if the liver became irreversibly damaged, but returned to 
normal levels if the damage could be reversed. If one liver lobe only 
was obstructed, the gastric hypersecretion occurred, but returned to 
normal if the resultant cirrhotic lobe was resected. The possibility 
of a gastric secretagogue from a damaged liver was proposed. 

Lerner and Thompson had suggested in 1963 (55) that Heparin 
was an inhibitor of gastric secretion. They discovered that the intra¬ 
venous administration of 100 mgm. of Heparin to adult dogs resulted in 
uniform inhibition of Heidenhain Pouch secretion following the stimulus 
of a test meal, the average percentage inhibition of free HCl being 
70%. In the same animals, the same dose of i/v Heparin resulted in an 
inhibition of Heidenhain Pouch secretion following Histamine stimula- 


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tion, the average percentage inhibition of free HCl this time being 
33%. They concluded that the binding of Histamine by Heparin both 
in vitro and in vivo was the mechanism of this action. In a paper 
published in 1965, Schulte and Ellison (56) noted that Heparin, in 
a dose of 2 mgm. per Kgm. body weight, had no predictable effect on 
maximal Histamine-stimulated gastric secretion. But in February, 1966, 
Thompson, Lerner, Tramontana, and Miller (57) showed a convincing and 
statistically significant inhibition of gastric secretion in all its 
phases on intravenous infusion of 10,000 U.S.P. units of Heparin. 

They reported the following decreases in gastric secretion as compared 
with control subjects; 


Antral phase; food stimulus... 74% 

Intestinal phase; good stimulus...... 71% 

Cephalic phase; insulin stimulus. 39% 

Antral phase; acetylcholine stimulus. 46% 

Mecholyl secretion. .. 44% 

Secretion stimulation by exogenous histamine.,.. 25% 
Secretion stimulation by exogenous gastrin. 40% 


The possible mechanism suggested was the binding of Heparin with 
Histamine in vivo or by preventing mast cell degranulation, but the 
evidence for this is circumstantial. The paper concludes by saying 
that there is still no role known for Heparin in gastric physiology. 
Histamine had been proposed as the common stimulant to gastric sec¬ 
retion, and several interrelations between Histamine and Heparin 
intrigued Thompson and his colleagues. 

By 1965, Gillespie and Grossman (58, 59), in a continuing 
series of experiments had confirmed the previously mentioned inhibitory 
effect on gastric secretion of cholecystokinin and secretion. His 








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further investigation of inhibitory raechanisms included data on duo¬ 
denal acidification, originally noted by Pavlov to diminish gastric 
secretion. The effect of acid in different parts of the alimentary 
tract now came under closer scrutiny by Grossman and his associates 
(60). They observed that acid instilled into the jejunum actually 
increased the volume of gastric juice secreted, while acid instilled 
into the ileum had no measurable effect on it. A series of experi¬ 
ments followed (61) in which they: (a) excised the pyloric sphincter, 

(b) transplanted the mid-duodenum together with the biliary and pan¬ 
creatic ducts into the jejunum, Cc) excised the duodenal bulb, and 
(d) removed the duodenum distal to the bulb, all of which resulted in 
an increased gastric secretion. Only total duodenectomy was found to 
abolish the increase. Andersson and Nillson (62), in the same year, 
showed that to inhibit the flow of gastric juice, the acid must be 
instilled into the region of the duodenal bulb, the distal part of the 

I 

duodenum being ineffective for this purpose. Acid reflux into the 
antrum may be the inhibitory mechanism in this instance. 

In 1966, the effect of fat in the duodenum was reappraised by 
Dibler, Harkins and Nyhus (63). The resultant inhibition was explained 
by either inactivation of circulating gastrin, or by direct action on 
the parietal cells; and the inhibition was noted to be reversed by 
pancreatic duct ligation, opening up a new field of inquiry. Grossman 
(64) has shown that an operation for bile exclusion, draining the 
common bile duct to the exterior, decreased the output of a Heidenhain 
Pouch. Going one stage further, Chey and Lorber (65), after reproducing 


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this inhibition by diverting the pancreatic secretion (or by pan¬ 
createctomy) , could restore the status quo by the instillation of fresh 
pancreatic juice into the duodenum, 

The phenomenon of gastric hypersecretion following resection of 
the small intestine, established by Landor and Baker earlier in the year 
(66 ), now came under scrutiny by Osborne and his co—workers later in 
1966 (67). Continuing experiments'showed that the rise in gastric se¬ 
cretion is proportional to the amount of intestine resected; that the 
parietal cell mass proliferates to increase the amount of basal secretion, 
occasionally to the extent of requiring gastric aspiration to deal with 
it. In one series, Osborne found that resection of the distal half of 
the small intestine stimulated a greater secretion in a Heidenhain Pouch 
than did a proximal resection. Stimulants and inhibitors of gastric se¬ 
cretion from the intestine were discussed, but the mechanism remains 
elusive. Either an inhibitor was removed, or a secretagogue was pro¬ 
duced. But which? 

A paper from Pennsylvania in July 1968 by Copeland, Miller, and 
Smith (68) has demonstrated once again significant increases in Heiden¬ 
hain Pouch secretion after isolation of parts of the small intestine, 
the maximal increase being observed when the duodenojejunal segment was 
removed from the food stream. While emphasizing the complex nature 
of control of gastric secretion by the small intestine, they made the 
important observation that their measured increases v^ere the same 
whether the isolated segment was left in situ as a mucous fistula, or 
removed entirely from the body. This is taken as evidence that the 
increase in gastric secretion is not produced by a secretagogue, but 


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16 


rather by the removal of an inhibitor. Support for this view is 
given by Kerr/ Elliott^ and Endahl this year (69 ), who used the same 
methods to produce the same results in dogs. These experimental 
findings are at variance with a recent paper by Salmon and Wright (70) 
with human subjects/ who showed a negligible rise in gastric secretion 
following massive small intestinal bypass in patients with obesity when 
the bypassed segment is left in situ as a mucous fistula, although the 
metabolic variation of these massively obese patients may invalidate 
any conclusion based on no 2 ano-somatic physiology. 

Both of these views'conflict with the findings of Westerheide, 
Elliott, and Hardacre (71), who, working from the same laboratory as 
Copeland, had shown in 1965 that an isolated and defunctionalized 
duodeno-'jejunal segment resulted in a greater acid production that 
that obtained by excising the same segment. Thus a spectrum of results 
is available, the two extremes being directly opposed to each other. 

The question of "secretagogue or inhibitor” remains under dis¬ 
cussion. In a series of ten dogs provided with bypass of different 
portions of the small intestine, Copeland (72) described three with 
ileal exclusion. Two of these dogs satisfied the criteria for 
secretagogue release, namely an increase in the submaximal and maximal 
Histamine response postoperatively, but the third did not, and he con¬ 
cludes that, since attempts at extraction of such a substance have 
failed, its existence is "problematic". He notes that the animal's 
absorptive surface will have diminished, and that substances like 
calcium, and bile salts, which are known to affect gastric secretion. 


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17 


and are absorbed through this surface, may play a role here by their 
relative absence. An interesting speculation here is the possibility 
of a decreased absorptive surface for an unknown substance having acid 
inhibitory potential. 

Both the Pennsylvania group and Kerr's team from Columbus, 

Ohio (73) feel that it is the removal of an inhibitor that is respon¬ 
sible for the increase, mainly on the basis that identical hyper¬ 
secretion is produced both by isolating and by excising the segment 
of small intestine. But the variability of this finding has already 
been mentioned. 

On the other hand, more convincing argument in favour of a 
secretagogue comes from the paper of Yakimets and Bondar in 1967 (74). 
They found that the gastric hypersecretion following small bowel re¬ 
section was reduced sharply on diverting the thoracic duct lymph— 
presumably the vehicle for the hormone—and restored on re-infusion of 
the lymph. Continuing this work, Chow (75) concluded that intact antral 
function was necessary for this phenomenon to occur, and that after re¬ 
section of some 65% of small intestine, secretagogues are carried in 
the thoracic duct lymph from the retained small or large intestine, and 
may act by potentiating antral gastrin, 

IV. Miscellaneous 

Visceral.-- The part played by the pancreas remains imperfectly 
elucidated, although experimental work has shown some surprising results, 
Dragstedt (76) has produced duodenal mucosal ulceration in 100% of dogs 








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18 


when he diverted their pancreatic ducts to the exterior, yet in 300 
pancreatectomies in dogs the incidence of ulcer was only 1.3%. He 
rejects Mann s explanation that the corrosrve action of the gastric 
juice on the duodenum is allowed to proceed without neutralization by 
the bicarbonate in pancreatic secretion, but admits the baffling nature 
of the phenomenon^ since in both cases the pancreatic secretion is 
equally absent. Noting that a ligated pancreatic duct gives a 20% 
duodenal ulceration rate, "occupying the middle ground", he hypothesizes 
some mechanism, presumably hormonal, which acts as a stimulant to the 
production of acid gastric juice, the intact antrum not being necessary 
for this phenomenon to occur. This and similar observations by other 
investigators has led to the hypothesis that the external secretion of 
the pancreas has the characteristic of preventing mucosal ulceration, 
while its internal secretion may play a part in the production of in¬ 
tractable "stress" ulcer (Curling's; Cushing's ulcer). 

Working on the assumption that gastrin may be partly destroyed 
or inactivated in the liver, Irvine and his associates (77) measured the 
Heidenhain Pouch secretion of animals before and after providing them 
with a portacaval shunt, and produced evidence in favor of this idea 
when he found the secretions raised postoperatively. His intact dogs 
were given doses of Histamine intra-jejunally that were insufficient to 
cause a raised Heidenhain Pouch secretion. This same dose was repeated 
following a portacaval shunt, when it produced a hypersecretion. One 
explanation is that Histaminase in the liver is bypassed by the operation 
but in a subsequent editorial, Irvine (78) concludes that this is only 





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19 


inferential, and that it is possible that the substance acting is 
gastrin. In 1960, Clarke (79) found that in human cirrhotics basal 
fasting and Histamine provocation tests were below normal in those 
without shunts, and not usually above normal in those with shunts. In 
the same year, a prospective study by Watkinson (80) revealed that in 
20,000 post mortem examinations, the incidence of peptic ulcer was 
higher in human cirrhotics., suggesting another mechanism than gastric 
hypersecretion for its production. 

Local factors .— The chronic ingestion of gastric irritants 
may ultimately lead to lesions attributable to secretory changes. 
Bacteria, swallowed from chronic nasopharyngeal foci; alcohol; condi¬ 
ments and spices; thermal trauma from food and drink; and improper 
mastication are examples of such agents, Although cigarette smoking 
has been shown to hinder the healing of peptic ulcer, the mechanism is 
not yet clear. Tobacco-charged saliva is a gastric irritant, and the 
systemic effect of nicotine on the autonomic nervous system may produce 
gastric symptoms. Endoscopic proof of "tobacco gastritis", however, is 
not available. 

Sundry drugs have been thought to produce gastritis, though in 
many cases the mechanism is obscure. Chief among the offenders are the 
salicylates and quinine derivatives. Extensive studies have convinced 
Menguy (81) and others that the effect of these drugs, and of cortico¬ 
steroids, on the gastric mucosa, is due neither to a local effect, nor 
to an increased gastric secretion—on the contrary, in dogs they de¬ 
crease’ the Heidenhain Pouch secretion—but to an impairment of the 




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20 

ability of the gastric mucosa to form its protective layer of mucus. 
Douthwaite (82) has observed the gastric mucosa following aspirin 
ingestion, and seen a range of effects of the hemorrhagic type, with 
small ulcers containing fragments of the drug. He concludes that 
possibly the anticoagulant property of the drug may play a part. A 
similar picture may be produced experimentally by the introduction into 
the stomach of Cinchophen. 

Other drugs implicated in the production of inflammatory and 
ulcerative lesions in the gastric mucosa are Phenylbutazone, Phenacetin, 
Indocid and others. 

In a recent article from Japan, Tobe, Fujiwara, and Muryobayashi 
(83) have notes that the effect of Serotonin is to cause intense angio¬ 
spasm, muscular spasm and ulceration in rat and mouse stomachs; furtner 
studies on this substance are expected to yield information of clinical 
importance. 

Work challenge.— In 1960, Card and Marks (84) showed that the 
output of gastric juice is proportional to the number of parietal cells 
in the fundus. The notion that the number of these cells could vary 
in an individual was propounded by Landor in 1964 (85), when he produced 
a work hyperplasia of them by continued physiological stimulation, and 
showed further that this process is reversible. On the same track, 
Eraslan and Hardy (86) repeatedly injected slowly-released Histamine 
into dogs, over a period of seven weeks, with the result that all gained 
weight, hypertrophied their gastric mucosa, and underwent an increase 
in the number of parietal cells. Similar treatment with Hydocortisone 



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21 

led to a slight decrease in the nximber of parietal cells, and growth 
hormone appeared to have no effect. 

In contrast, stomachs with a low acidity have been found to 
possess fewer parietal cells; this is seen in such diseases as carcinoma 
of the stomach, pernicious anaemia, chronic gastritis, acute fevers, 
malnutrition, gallbladder disease, Addison's disease, sprue, acne 
roseacae and chronic arthritis. 

It is the opinion of Dragstedt (87) that the protracted physio¬ 
logical challenge producing this hypersecretion is a persistence of the 
vagal mechanism acting at an inappropriate time which, if true, lends 
support to the theory of an "ulcer personality". 

V. Conclusion 

As knowledge about gastric secretion accumulates, it is becoming 
increasingly clear that the traditional Pavlovian "phases" are not dis¬ 
crete. This structure would hinder the further understanding of this 
subject if rigidly imposed on the thinking since the phases do not work 
in isolation. The delicate interweaving of the different agents as they 
act on their target organ requires that they be understood in terms 
of each other, as well as in their own direct action on the stomach. In 
this way, such apparent paradoxes as the simultaneous stimulation and 
inhibition of secretion after vagal stimulation will be resolved, just 
as the duality of action of the antrum was understood by recourse to 
the other mechanisms. 

As the traditional theory gives way to a new pattern of thinking, 
having served its purpose, so new practical methods replace the 







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tline—honoured ones that have contributed so much information over the 
years. The sole method of collecting gastric secretions in the intact 
human subject has been by nasogastric aspiration of stomach contents, 
usually after a test meal. The value of this as an indication of 
regular intra-gastric events in the subject is limited, for the follow¬ 
ing reasons. In order not to block the aspiration tube, the test meal 
is usually liquid, whereas the normal human diet is a mixture of solid 
and liquid. Liquid alone takes a different intra-gastric course, and 
leaves the stomach more rapidly than a meal of solid food, thus stimula¬ 
ting its secretions for a different length of tim.e. 

The liquid in question must be free of protein, because protein 
will act as a buffer, and distort the pH. It must be fat-free, because 
fat in the duodenum depresses acid secretion; and the carbohydrates 
must be of a high molecular weight, and stable in the stomach, in 
deference to their osmotic capabilities. 

S. J. Rune (88), in his current monograph from Copenhagen, has 
outlined these shortcomings, and shown that the customary test meal 
acts mainly as a volumetric stimulus, and is a weaker one than solid 
food. Moreover, since its emptying is exponential, the intra-gastric 
stimulus rapidly declines. Its inevitable lack of buffering capacity 
briskly leads to a high acid level in the antrum, which in turn artifi¬ 
cially depresses gastrin release. Aspiration of the stomach contents 
for analysis gives only a spot reading, and concludes the test. Should 
other readings be required at different intervals following the test 
meal, the entire procedure must be repeated, and variables are introduced 


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Runs piroposBS a. novsl rncthod of avoiciinp all th.GSB pitfalls, 
in which unlimited serial readings are taken after a realistic meal 
of solid food, without disturbing the stomach contents. The readings 
taken from a fraction of the peripheral blood, and the principle 
behind the method is that acid lost from the parietal cells will alter 
the organism's acid/base balance proportionately. Base excretion in 
the urine and bicarbonate secretion from the pancreas are compensated 
for in the equation, which is simply; gastric acid secretio n = net 
acid loss + base excretion in ur ine + pancreatic bicarbonate secretion. 

Results with this indirect method have proved encouraging, and 
Rune's investigations have invariably shown an increase of the base 
concentration in arterial blood after the consumption of a major meal 
preceded by a twelve-hour fast in patients with normal gastric acid 
secretion. This increase was not found in patients with achlorhydria 
or low secretory capacity. It seems likely that more sensitive studies 
will be possible with this method as research continues in this field, 
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FOOTNOTES 


1 

BEAUMONT, W. Experiments and observations on the gastric 
juice and the physiology of digestion. Plattsburg, F. P, Allen, 1833. 

2 

BLONDLOT, N. Sur le principe acide du sue gastrique. 

J. de la physiol, de I'hoinme, ^:308-320, Par. 1858. 


CARLSON, A.J. The secretion of gastric juice in health and 
disease. Physiol. Review, ^:l-40, 1923. 

4 

WOLF, A., and WOLFF, H.G. Human gastric function. Ox. Un. 
Press, 1943. 


5 

PAVLOV, I.P., and SCHUMANN~SIMANOVSKAJA, E.O. Die Innervation 
der Magendrusen beim Hunde. Arch. f. Physiol. Leipz., 1895. 


RICHET, C. Des proprietes chimiques at physiologiques du sue 
gastrique chez I'homme et les animaux. J. de I'anat. et physiol, etc., 
xiv :170-333. Par. 1878. 


7 

UVNAS, B. The part played by the pyloric region in the 
cephalic phase of gastric secretion. Acta. Physiol. Scand. 4 (Suopl. 13), 
1942. 


8 

BENNETT, T.I., and VENABLES, J.F. The effects of emotions on 
gastric secretions and motility in the human being. Brit. M. J., 
London, (i):662, 1920. 


9 

GROSSMAN, M.I. Cholinergic potentiation of the response to 
gastrin. J. Physiol., 157:14P, 1961. 


10 

BEDFORD, M., SAVAGE, L.E., and SCHOFIELD, B. The blocking of 
gastrin release. J. Physiol., London, 162:6lP, 1962. 


RUNE, S.J. The metabolic alkalosis following aspiration of 
gastric acid secretion. Scand. J. Clin, and Lab. Inv., 17;305-310, 
1965. 















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25 


12 

DRAGSTEDT, L., WOODWARD, E.R., STORER, E.H,, OBERHELMAN, H.A., 
and SMITH, C.A, Quantitative studies on the mechanism of gastric 
secretion in health and disease. Ann. Surg., 132:626, 1950. 

13 

DRAGSTEDT, L.R, Gastrin and peptic ulcer. Arch. Surg., 
91:1005-1010, Dec. 1965. 

14 

EMAS, S., and GROSSMAN, M.I. Difference between dogs and 
cats in effect of large dose of gastrin on gastric secretion. 
Physiologist, ^:175, 1966. 

15 

FRENCH, J.D., LONGMIRE, R.L., PORTER, R.W., and MOVIUS, H.J. 
Extravagal influences on gastric hydrochloric acid secretion induced by 
stress stimuli. Surgery, 3^:621, 1953. 

16 

MASON, G.R., and NELSEN, T.S. Hypothalamic stimulation and 
gastric secretion in the dog. Am. J. Physiol., 213 :21, 1967. 

17 

DRAGSTEDT, L.R. II, JOHNSON, A.N. Jr., SINGER, E.R., and 
OBERHELMAN, H.A. The effect of vagotomy on the intestinal phase of 
gastric secretion. Surg. Forum, 11:336, 1960. 

18 

STORER, E.H., SCHMITZ, E.J., SALVAGE, L.R., KANAR, E.A., 
DIESSNER, E.H., and HARKINS, H.N. Gastric secretion in Heidenhain 
pouches following section of vagus nerves to main stomach. 

Proc. Exp. Biol, and Med., 325-327, 1952. 

19 

NYHUS, L.M., CHAPMAN, N.D., DeVITO, R.V., and HARKINS, H.N. 

The control of gastrin release. Gastroenterology, 39_:582, 1960. 

20 

PEVSNER, L., and GROSSMAN, M.I. The mechanism of vagal 
stimulation of gastric acid secretion. Gastroenterology, _^:493, 1955. 

21 

EDKINS, j.S. The chemical mechanism of gastric secretion. 

J. Physiol. (London), 3^:133-144, 1906. 

22 

BAYLISS, W.M. Principles of general physiology (3rd edition), 
p. 344, Longmans, Green and Co., London, 1920. 

23 

ANDERSSON, S. Inhibitory effect of hydrochloric acid in 
antrum and duodenum on gastric secretory responses to rest meal in 
Pavlov and Heidenhain pouch dogs. Acta. Physiol. Scand., 49_:231, 1960. 




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SIRCUS, W. Studies on the mechanisms in the duodenum in¬ 
hibiting gastric secretion. Quart. J. Exp. Physiol., £^:114, 1958. 

25 

HARRISON, R.C., LAKEY, W.H., and HYDE, H.A. The production 
of an acid inhibitor by the gastric antrun\. Ann. Sur., 144:441, 1956, 


POPIELSKI, L. Die Wirkung der Organextrakte und die Theorie 
der Hormone. Muncher med. Wehnschr., 59:534, 1912. 

27 

LIM, R.K.S., IVY, A.C., and MCCARTHY, J.E. Contributions to 
the physiology of gastric secretion. I. Gastric secretion by local 
(mechanical and chemical) stimulation. Quart. J. Exp. Physiol., 

15_:13, 1925. 

28 

DUVAL, M.K., Jr., and PRICE, W.E. The mechanism of antral 
regulation of gastric secretion: discontinuous cross circulation. 

Ann. Surg., 153:581, 1961. 


29 

LIM, R.K.S., and MOZER P. Mechanism of excitation of 
internal secretion of pylorus and adenteric reflex. Am. J. Physiol., 
163:730, 1950. 


30 

GREGORY, R.A,, and IVY, A.C, The humoral stimulation of 
gastric secretion. Quart. J. Exp. Physiol,, ^:111, 1941. 

31 , . , . . ^ 

BERGSTROM, H., and BROOME, A. Preoperative determination of 

the boundary between the gastric antrum and fundus. Acta. Clin, 
Scand., 128:526-529, 1964. 


32 

RUDING, R., and HIRDES, W.H. Extent of the gastric antrum 
and its significance. Surgery, _^:743-755, June, 1963, 

33 

DRAGSTEDT, L.R., WOODWARD, E.R., OBERHELMAN, H.A. STORER, E.H., 
and SMITH, C.A. Effect of transplantation of antrum of stomach on 
gastric secretion in experimental animals. Am. J. Physiol,, 165 :386- 
398, 1951. 

^"^DUVAL, M.K., Jr., and PRICE, W.E. The mechanism of antral 
regulation of gastric secretion: continuous cross circulation. 

Ann. Surg,, 152:410, 1960. 


35 

THOMPSON, J.C., TRAMONTANA, J.A., LERNER, .J.H., and 
STALLINGS, J.O. Physiologic scope of the antral inhibitory hormone. 
Ann. Surg., 156:550, 1962. 













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36 

GILLESPIE, I.E., and GROSSMAN, M.I. Inhibition of gastric 
secretion by extracts containing gastrin. Gastroenterology, 44:301- 
310, 1963. ■ 

37 

MENGUY, R.B., MASTERS, Y.F., and GRYBOSKI, W.A. Isolation 
of a gastric inhibitory substance in canine gastric juice. Surg. 
Forum, 14:951, 1963. 


38 

WORMSLEY, K.G., MAHONEY, M.P., and NG, M. Effects of a 
gastrin-like pentapeptide (ICI 50, 123) on stomach and pancreas. 
Lancet, 1:993, 1966. 


39 

SCHOFIELD, B., RED FORD, M., GRABIIAM, A.H,, and NUIAMI, K. 
Neural factors in the control of gastrin release. Symposium on gastric 
secretion (Edmonton, Alberta, Canada). Pergamon Press, (1st edition), 
p. 91, 1967. 

40 

LECONTE, P. Cellule. 17:307, 1900. 

41 

PAVLOV, I.P. Work of the digestive glands, London, 

Charles Griffin and Company, 1910. 

42 

SOKOLOV, A.P., Thesis, St. Petersburg, 1904. Quoted by 
Babkin, B.P. Secretory mechanism of the digestive glands. New York, 
Paul B. Hoeber, Inc., 1950. 

43 

BAYLISS, W.M., and STARLING, E.H. The mechanism of pancreatic 
secretion. J. Physiol., 28:325, 1902. 


44 

FA_RRELL, J.I., and IVY, A.C. Studies on the motility of the 
transplanted gastric pouch. J. Physiol., 1^.221, 1926. 

45 

KOSAKA, T., and LIM, R.K.S. Demonstration of the humoral 
agent in fat inhibition of gastric secretion. Proc. Soc. Exp. Biol., 
N.Y., 27:890-891, 1930. 


46 

IVY, A.C., and OLBERG, E. Observations on the cause of 
gall bladder contraction and evacuation. Proc. Soc. Exp. Biol, and 
Med., 25:251, 1928. 


47 

ANDERSSON, S. 


Handbook of Physiology. Amer. Phys. Soc., 1967. 




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59 

GILLESPIE^ I.E., and GROSSMAN, M.I. Inhibition of gastric 
secretion by extracts containing gastrin. Gastroenterology, 44-301- 
310, 1963. - 

60 

KONTUREK, S., and GROSSMAN, M.I. Localisation of the 
mechanism for inhibition of gastric secretion by acid in intestine. 
Gastroenterology, £9:74, 1965. 

61 

KONTUREK, S., and GROSSMAN, M.I. Localisation of the 
mechanism of inhibition of gastric secretion by acid in intestine. 
Gastroenterology, 49:74, 1965 

62 

ANDERSSON, S., NILSSON, G., and UVNAS, B. Inhibition of 
gastric secretion by acid in proximal and distal duodenal pouches. 
Acta. Physiol. Scand., £5:191, 1965. 

63 

BIBLER, D.D., Jr., HARKINS, H.N., and NYHUS, L.M. 

Inhibitory effect of fat in the duodenum and upper small intestine on 
exogenous gastrin stimulated gastric secretion. Surgery, 60, 4:844- 
847, October, 1966. ~ 

64 

NAHRWOLD, D.L., and GROSSMAN, M.I. Effect of exclusion of 
bile from the intestine on gastric acid secretion. 


65 ' 

CHEY, W.Y., and LORBER, S.H. Influence of pancreas on gastric 
secretion in dogs. Am. J. Physiol., 212(2) ;252-260, 1967. 

66 ^ , 

LANDOR, J.H., and BAKER, W.K. Gastric hypersecretion 
produced by massive small bowel resection in dogs. J. Surg. Research, 
4_:518, 1964. 

67 

OSBORNE, M.P., FREDERICK, P.L., SIZER, J.S., BLAIR, D., 

COLE, P., and THOM, W. Mechanism of gastric hypersecretion following 
massive intestinal resection, clinical and experimental observation. 

Ann. Surg., 164 :622-634, 1966. 

68 

COPELAND, E.M., MILLER, L.D., and..SMITH, G.P. The complex 
nature of small bov/el control of gastric secretion. Ann. Surg., 

168 :36-45 , July, 1968, 

69 

KERR, G., ELLIOTT, D.W., ENDAIL, G.L. Effect of antrectomy on 
gastric acid hypersecretion induced by isolation of the proximal small 
bowel. Amer. J. Surg., 115 :157-164, February, 1968. 






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29 


70 

SALMON, P.A., and WRIGHT, W.J. Effect of small bov;el bypass 
on gastric secretion in obese patients. Canad. J. Surg., 11:365-368, 
July, 1968. 

71 

V7ESTERHEIDE, R.L., ELLIOT, D.W., and HARDACRE, J.M. The 
potential of upper small bowel in regulating acid secretion. Surgery, 
^:73, 1965. 

72 

COPELAND, E.M., MILLER, L.D,, and SMITH, G.P. The complex 
nature of small bowel control of gastric secretion. Ann. Surg., 
168:36-45, July, 1968. 


73 

KERR, G., ELLIOTT, D.W., ENDAHL, G.L. Effect of antrectomy 
on gastric acid hypersecretion induced by isolation of the proximal 
small bowel. Amer. J. Surg., 115:157-164, February, 1968. 


74 

YAKIMETS, W.W., and BONDAR, G.F. The effect of complete 
thoracic duct lymph diversion on gastric secretion in dogs. Canad. 

J. Surg., ]^:218-222, 1967. 

75 

CHOW, K.Y. Effect of enterectomy on gastric secretion. 

M.Sc. thesis. University of Alberta, Edmonton, Alberta, Canada. 

June, 1968. 

V 6 

°DRAGSTEDT, L.R. Pathogenesis of gastroduodenal ulcer. 

Arch. Surg., ££: 438-451, March, 1942. 

"^"^IRVINE, W.T., DUTHIE, H.L., RITCHIE, H.D., WATON, N.G. 

The liver's role in histamine absorption from the alimentary tract. 
Lancet, 1^:1064, 1959. 

70 

IRVINE, W.T. The liver, gastric secretion and histamine. 
Gastroenterology, 4^:337-339, March 1962. 

"^^CLARKE, J.S., HOFFS, M., ELFARRA, S. The effect of portacaval 
transposition on Heidenhain pouch secretion in response to various 
stimuli. Surg. Forum, ]^: 134-138, 1960. 

^^WATKINSON, G. The incidence of chronic peptic ulcer found 
at necropsy; a study of 20,000 examinations preformed in Leeds in 
1930-49 and in England and Scotland in 1956. Gut, ]^:14, 1960. 






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48 

BABKIN, B.P. Die aussere Sekretion der Verdauungsdrusen 
(2nd edition). J. Springer, Berlin, 1928. 

49 

BEAMER, W.D., FRIEDxMAN, M.H.F,, THOMAS, J.G., and REPiFUSS, 
M.F. Factors responsible for the intestinal phase of gastric 
secretion. Am. J. Physiol., 141 :613-618, 1944. 


50 ^ 

ERSPAMER, V., and ASERO, B. Identification of enteramine 
the specific hormone of the enterochromaffin cell system, as 5— 
Hydroxytryptamine. Nature, London, 169 :800, May, 1952. 

51 

OLSON, T.E., and GRAY, S.J. Serotonin and gastroenterology. 
Am. J. Gastroenterology, 29:280-289, 1958. 


BLACK, J.W,, FISHER, E.W., and SMITH, A.N. The effects of 
5-Hydroxytryptamine on gastric secretion in anaesthetised dogs. 

J. Physiol., 141:27, 1918. 


RESNICK, R.H., and GRAY, S.J. Distribution of serotonin 
(5~Hydroxytryptamine) in the human gastrointestinal tract. Gastro¬ 
enterology, _41:119, 1958, 

54 

SILEN, W., HEIN, M.F., ALSO, R.J., and HARPER, H.A. 
Influence of liver upon canine gastric secretion. Surgery, 54:29-36, 
July, 1963. ~~ 

55 

LERNER, H.J., and THOMPSON, J.C. Heparin suppression of 
gastric acid secretion. Soc. Exp. Biol, and Med., 112:3, 730, 

March, 1963. 


SCHULTE, W.J., and ELLISON, E.H. Heparin suppression of 
histamine stimulated gastric secretion. Surg. Forum, 16:311-312, 
1965. 


57 

THOMPSON, J.C., LERNER, H.J., TRAMONTANA, J.A., and 
MILLER, J.H. Range of action of heparin in suppressing canine gastric 
acid secretion. Surg. Gyn. and Obst., 122 :264-268, 1966. 

58 

GILLESPIE, I.E., and GROSSMAN, M.I. Inhibitory effect of 
secretin and cholecystokinin on Heidenhain pouch responses to gastric 
extract and histamine. Gut, 342-345, 1964, 








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81 

MENGUY, R. Editorial. Gastroenterology, 51:430-432 
September, 1966. — ' 

82 

DOUTHWAITE, A.H., and LINTOTT, G.A.M. Gastroscopic 
observation of the effect of aspirin and certain other substances on 
the stomach. Lancet, 235:1222, November, 1938. 

83 

TOBE, T., FUJIWARA, M., and MURYOBAYASHI, T. Ulcerogenic 
effect of 5-Hydroxytryptamine (serotonin) in the stomach. Ann. Surg , 
166:1002, 1967. 


84 

CARD, W.I., and MARKS, J.N. The relationship between the 
acid output of the stomach following maximal histamine stimulation 
and the parietal cell mass. Clin. Sci., 19:147, 1960. 

85 

LANDOR, J.H., PORTERFIELD, J.F., and WOLFF, W.S. Correlation 
of parietal cell population with the level of gastric secretion in dogs 
with Heidenhain pouches. Surg. Forum, 15:310, 1964. 

86 

ERASLAN, S., and HARDY, J.D. Chronic stimulation of the 
gastric parietal cell mass. J. Surg. Research, 6:157-141, March, 1966. 

87 

DRAGSTEDT, L.R., RAGINS, H., DRAGSTEDT, L.R., II,, and 
EVANS, S.O., Jr. Stress and duodenal ulcer. Ann. Surg. 144:450, 1956. 

88 

RUNE, S.J., and LASSEN, N.A. Diurnal variations in the acid- 
base balance of blood. Scand. J. Clin. Lab. Invest., 2.2:151-156', 1968. 




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METHODOLOGY 


I. General 

Adult mongrel dogs of both sexes and weighing 11 - 15 kg. were 
used. All animals were kept at the Health Sciences Animal Center, 
Ellerslie, Alberta, for two weeks before being released to the labora¬ 
tory, during which time they were immunized with distemper vaccine, 
canine hepatitis vaccine, dewormed, and given any other special treat¬ 
ment necessary for the maintenance of good general health. Pregnant 
dogs were not used, and those which became ill or pregnant during the 

course of the experiments were excluded from the results. 

* 

The dogs were fed on commercial dog food according to size, 
the average being fourteen ounces per dog per day. Unrestricted 
water was supplied. The dogs were exercised daily in outdoor runs. 

II. Experimental Plan 

Heidenhain Pouches were constructed on twelve dogs, and three 
weeks allowed for the recovery period before the secretions were 
measured repeatedly on all dogs under the following six sets of con¬ 
ditions. 

1. Twenty-four hours fed, awake. 

2. Twenty-four hours fasting, awake. 

3. Eight hours fed, awake. 

4. Eight hours fasting, awake, 

5. Eight hours fed, asleep. 

6. Eight hours fasting, asleep. 

* 

Dr. Ballard's 


32 





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Once this baseline was established, the dogs were divided into 
two groups of six—Group A, and Group B. Group A underwent resection 
of 55% of the small intestine just distal to the Ligament of Treitz, 
with end-to-end anastomosis (proximal enterectomy); Group B had 55% of 
the small intestine removed just proximal to the ileo-caecal valve, 
again with an end-to-end anastomosis (distal enterectomy). 

After a recovery period of three weeks, Heidenhain Pouch 
secretions v/ere again measured under the same six sets of conditions. 

The final stage of the experiment was supra-diaphragraatic 
cannulation of the thoracic duct, diversion of its contents into a 
heparinized collecting vessel for four hours, followed by reinfusion of 
this lymph over the next two hours. After a thoracotomy, Heidenhain 
Pouch secretions were measured for two hours to establish a baseline. 

The anaesthetized dogs were then fed a measured quantity of food by 
orogastric tube (120 gm. of meat homogenized in 80 ml. distilled water), 
and the thoracic duct lymph simultaneously diverted for the next four 
hours. This lymph was reinfused into a systemic vein for the following 
tv;o hours, at the end of which time, the animals were sacrificed. This 
procedure was carried out on the dogs of both groups. 

Ill. Before Operation 

The animals were exercised normally up to the day of operation. 
Twenty-four hours of fasting from food and twelve from water preceded 
the operation. If examination of the animal before operation showed 
any abnormality, the procedure would be delayed until it was remedied; 
or the dog excluded from the series. 









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IV. Operation 

The animals v/ere anaesthetized with intravenous Nembutal, 
C’Diabutal") 30 mg./kg. body weight, and intubated with a cuffed endo¬ 
tracheal tube. The hair was shaved from the abdomen, and the under¬ 
lying skin washed with surgical soap and water. The dog was then placed 
in the supine position on the operating table, where the legs were 
secured by a tether from each corner of the table and an intravenous 
solution of 5% dextrose saline started at 5 ml./kilo./hour. The 
operative site prepared with "Betadine" iodine solution. For the intra¬ 
abdominal procedures, a midline incision was used to facilitate a re¬ 
latively bloodless entry; this was placed cephalad for Heidenhain Pouch 
construction, and more caudad for the enterectomies. Strict asepsis was 
maintained at all times. 

V. Heidenhain Pouch Construction (Figure 1) 

After suitable preparation, the abdomen was opened, and a 
survey made of the tissues to exclude any pathological condition. If 
the spleen was large and bulky, it was exteriorized in moist sponges, 
to facilitate exposure and delivery of the stomach. 

Gentle traction caudad on the greater curvature of the stomach 
permitted its delivery into the wound, where it v/as stretched out and 
flattened. The omentum v/as gently lifted off the upper surface, and 
non-crushing clamps applied in such a way as to isolate a large wedge 
of the organ from the greater curvature. The wedge was fashioned from 
the tissue of the proximal fundus, to avoid including significant 
amounts of antral mucosa. The point of the wedge v/as not allowed to 






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HEIDENHAIN POUCH 


Fig, 1.—Heidenhain Pouch 



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36 

approach the lesser curvature too closely, to avoid producing a con¬ 
striction in the body of the remaining stomach. 

Before the clamps were removed from the main stomach, the cut 
edges of mucosa were joined with 3-0 chromic catgut, and this suture 
line buried with another 3-0 chromic catgut in the serosal layer. 

Before closure of the pouch, a stainless steel cannula was inserted, 
and brought out through a stab-wound away from the suture line. The 
cut edges of the pouch were then sewn together in the same way as those 
of the stomach, and the end of the cannula brought out through a stab- 
wound in the abdominal wall. The pouch v/as fixed in this position by 
several sutures between serosa and the tissues of the internal abdominal 
wall. Thus, pouch contents could be collected by applying a bag to the 
exteriorized part of the cannula, v/hich would drain gastric secretions 
continuously. 

VI. Proximal Enterectomy (Figure 2) 

The total length of the small intestine, exteriorized on moist 
sponges, v/as measi;red with a ruler, the average being 300 cm. from the 
Ligament of Treitz to the ileocecal valve. 

Measurement of the length to be resected was started at a point 
5 cm. distal to the Ligament of Treitz. Markers were applied both here 
and at a point about 165 cm. (i.e. 55%) distal to this, delineating the 
amount to be resected, and non-crushing clamps were applied to the bowel 
wall at these points. The mesenteric vessels lying between these two 
points were ligated in continuity with 4-0 silk and divided between the 
ligatures. The intermediate intestine was then resected, to include 




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Fig. 2.—55% Proximal Enterectcmy 







38 


the cuff that was clamped and continuity restored with a two layer 
end-to-end anastomosis, 5-0 chromic being used for the mucosa and 4-0 
silk for the serosa. The mesenteric defect was then closed with 4-0 
chromic sutures to prevent subsequent herniation. The abdominal wound 
was then closed in layers using an absorbable subcuticular stitch for 
the skin to obviate the need for suture removal during the recovery 
period. 

VII. Dist al Enterectomy (Fi gure 3) 

The procedure used for this operation differed from that used 
for a proximal enterectomy only in that the resected intestine was 
measured cephalad from a point 5 cm. proximal to the ileocecal valve. 

VIII. Thoracic Duct Cannulation 

After endotracheal intubation with a cuffed tube which was then 
connected to a positive pressure ventilator, an intravenous solution of 
5% dextrose saline was started at 5 ml,/kilo .'/hour. 

A right-sided thoracotomy was then performed with the dog lying 
on his left side. Exposure was maintained with a rib retractor, and 
the right lung was packed out of the field with moist sponges. Simul¬ 
taneously with the thoracotomy, a Bard rubber bladder was attached to 
the cannula from the Heidenhain Pouch, and secretions measured hourly 
for two hours to establish a baseline before any further surgery was 
undertaken. 

At the end of this tv;o hour period, an incision was made in the 
parietal pleura overlying the aorta, and the thoracic duct identified 
as it lay in the dorsal sulcus alongside. The duct was ligated at its 








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HEIDENMAIN POUCH 



Fig. 3.—55% Distal Enterectomy 



40 


cephalad end in the field, to suffuse it with lymph and increase its 
calibre, and a silastic catheter threaded into it through a small 
incision. The catheter was passed caudally for its tip to lie in the 
cisterna chyli. At the same time the dog was fed 120 gm, of meat 
(Dr. Ballard's dog food) homogenized with 80 ml, of distilled water, 
through an orogastric tube. 

The open end of the catheter was then brought out of the chest 
wound, and allowed to drain into a sterile graduated cylinder placed 
on a lower level than the chest to obtain a siphon effect. The rib 
retractor and packs were then removed, and the wound temporarily closed 
with towel clips and a sterile cover. Five hundred units of Heparin 
were added to the lymph draining into the cylinder to prevent clotting, 
and hourly recordings made of the volume of the lymph in the cylinder, 
and the Heidenhain Pouch secretions in the bag. 

Four hours after the start of this collection, the intravenous 
infusion of 5% dextrose saline was stopped. An intravenous infusion 
was simultaneously started with this collected lymph, infused at the 
same rate over the next two hours. Measurements of Heidenhain Pouch 
secretion were continued in the same way. At the end of this two hour 
period, the procedure was terminated and the dog sacrificed, 

IX. Postoper ative Management 

Parenteral fluids were given for three days following surgery, 
as 30 ml./kg. of 5% dextrose saline intravenously for the first day, 
and subcutaneously for the next two. After the third day the dog was 
permitted to drink water, then milk and pabliam or Heinz clear consomme 
of soup for two days. By the sixth day the dog was invariably back on 



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a normal diet. 

Parenteral antibiotic was used prophylactically during surgery, 
and the immediate postoperative period, as 2 ml, of "Fortimycin" (a 
mixture of 400,000 I,U, penicillin and 0.5 gm, dihydrostreptomycin). 

The first dose was given on the morning of the surgery, and then daily 
until the third postoperative day. Normal exercise was resumed at 
this time. 

Following enterectomy, the dog was given 1 gm. of calcium 
carbonate orally when normal feeding was resumed, to avoid problems of 
diarrhea. This has been shown to be due to the detergent property of 
the soaps irritating the intestinal mucosa. The insoluble calcium soap 
is precipitated, restoring the physiological nature of the luminal 
content. Negligible absorption of calcium takes place in the shortened 
intestine, and no hypercalciuria has been shov/n in animals fed up to 
30 gm. of calcium (1). A minimum period of three xveeks was allowed 
between the conclusion of the surgery and the beginning of any further 
measurements of Heidenhain Pouch secretion. 

No special therapeutic measures, such as transfusion, were 
necessary during the postoperative period, 

X, Collecti on of Samples 

For the twenty-four hour collections the bladders were fitted 
on at 5;00 p.m, on one day, and removed with the secretions at 5;00 p.m. 
on the next. Normal activity was permitted during this period, with 
the exception that the dogs were muzzled to avoid their damaging the 
bladders. For the fed collections the muzzles were removed to allow 
the dogs to eat; and then replaced. 




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42 


The food consisted of eight ounces of commercial dog food given 
twice daily; for the fasting collections only water was given as 
required. 

For the eight hour collections, the same techniques were used 
on the conscious dogs, except that the collections were measured hourly. 
For the sleeping collections the animals were anaesthetized with intra¬ 
venous Nembutal ("Diabutal") 30 mg./kg., and an endotracheal tube in¬ 
serted. They were laid on their left side with the cannula and rubber 
bladder dependent, and intravenous 5% dextrose saline infused at a rate 
of 5 ml,/kg,/hr. Heidenhain Pouch secretions were collected and measured 
hourly. In the anaesthetized fed collections, 120 gm, of commercial 
dog meat was homogenized with 80 ml. of water, and given through an oro- 
gastric tube at the end of the second hour. 

In all collections, the bladders were carefully inspected for 
any damage or leakage, and that collection discarded if any were dis¬ 
covered . 

XI, D etermination of Gastric Acidity 

The volume of every sample was first measured and recorded. The 
amount of free and total acid in the secretions was determined for every 
sample by the follov/ing method; one milliliter of the sample was 
pipetted into a titration vessel in an autoburette, and the pH measured 
automatically and indicated on a pH meter. 

The radiometer automatic titrator was then connected to the 
autoburette, and N/10 sodium hydroxide automatically added to the .sample 
until a pH of 4.0 was reached, at which time the amount of free acid 


was indicated on a dial on the autoburette. 






1 , t 


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7 


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- ai,.vi 


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' i-i-Mix'lli'1-1 ('"...ii.iH'.. 







43 


At this point another circuit was set in operation, which 
continued the titration to pH 7.0 when the amount of total acid appeared 
on the same scale on the autoburette. 

No indication was used, because the amount of N/10 sodium 
hydroxide added to bring the pH to four and seven respectively was 


directly proportional to the amounts of free and total acid present. 


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* i- / ' ■ ♦ 


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„‘w N’f ' 



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FOOTNOTES 


^LeVEEN, H.H., BOREK, B., AXELROD, D.R., and JOHNSON, A. 
Cause and treatment of diarrhea following resection of the small 
intestine. Surg. Gyn. Obst., 124:766, 1967, 







RESULTS 


I. First Stage 

Control values of Heidenhain Pouch secretion were established on 
twelve dogs, under the following conditions: 


1. Twenty-four hours awake fed ) 

2. Twenty-four hours awake fasting ) 

3. Eight hours awake fed 

4. Eight hours awake fasting 

5. Eight hours anaesthetized fed 

6. Eight hours anaesthetized fasting 


(one collection) 


(hourly collections) 


Six of these dogs subsequently underwent a 55% proximal enter- 
ectomy (Group A), and the remaining six a 55% distal enterectomy 
(Group B). Heidenhain Pouch secretions were again measured under 
identical conditions. These were examined for volume, pH, concentration 
of total acid, and concentration of free acid. In order to avoid 
giving a falsely high impression of the gastric acidity of dogs with a 
small Heidenhain Pouch secretion, the acidity is expressed in units of 
m.Eq./volume rather than m.Eq./litre. 


Twenty-Four Hour Measurements 

After enterectomy, both groups secreted a greater volume of 
gastric juice and acid when fed than the controls (Figure 4). Group A 
showed a 73% increase in volume, and Group B, a 66% increase (Table 1). 

■k 

Both these increases were statistically significant at 5% (p = 0.05) 
(Tables 11 and 12). 

* 

Statistical analysis (Tables 11-28) appear at the end of this section. 


45 




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• 


no i . i>j£a ij Utl-- 'i<> v-'t/l.iv io'a.ifto^ 





f; 






»4nf>i fir V*v^- llT.4Wt«M - 5 fnii 

' " ; 4 ' 

I * tcfclf z'-iO'uf 7Slf<lii“Y,'*t«..*W'^ (|S I , j 

{ ti»5 *t ' 

, ( «Tudrf .^ 

tv'* ’■') h^'^' fXiiCiH ^tfpzJ .2' 

' ' '"X p,rl:/t.4^ rc •<£! »uwtd : 

' f' 

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^ s I i^.i 

M'•r:j^ f.is’ Idtr , iA ?JWc»;tOd' 



(• 'M' ai 


-fr^t'^rw ' . n ‘-ijj (tit t ' s.>’ »‘Ji <? iili»<*U{tii >'.}^i i t«. qfio:»3) 

' ' ■ * . ■ . !l 

n:jl>8:i3n>/mv’ .”'; h-- i* .' <j^> XAoi.3nf*bi , 


. '• 'O' ^ '- ’{s -^ 

-iJ r..T .[ft rn - ■ j^- ,Wt‘n 3o 


i.M ,< 


;>uj Ilf •'<'^ s J ’'*’ 



'. f. ,l.^* , no.fcj fj'we bv'®! nii»! XJ*/rm' 


•. I' 


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, <i, nfriaT) 888r-.‘^ /tl (Trt^ r ,“i tiiM'tl? fc«? v»«aut<^v oHMtonl 01X t ew«*vK)rte 

t£0«0 x <^ 88 yl 1U*U3A.'^8 sinv ^vt%no:ionl ni^ocii fflofl 

■ j,, iil. 

' . " ■ 4 i, ' 


'a.. 


■ Vk ' I 


III I'p ^|^il■^■ H 


.ooJWoftii »itis 510.1108 cwbif’C. tJf. aairtflTji eX^t-fwiA X8;^4:^8i4*32 

. - . . *,, ' } , . -''‘-v 

■ ' -=.. •" '' 


L^'JaJlA i' it 


. 





» 


'i'-ii 


j a'' 




•f^' 



J 





Fig. 4.—Comparison of the mean twenty-four hour postprandial Heidenhain Pouch 
secretion in control dogs, and enterectonized Group A and Group B dogs. Secretion 
was significantly increased in both groups (p = 0.05). Free and total acid was 
significantly increased (p = 0.05) in Group A dogs, but not in Group B dogs. 
























































































47 


TABLE 1.—Mean Total Postprandial Heidenhain Pouch Secretions in 
Control Dogs, Dogs with 55% Proximal Enterectomy 
(Group A), and Dogs with 55% Distal Enterectomy 
(Group B). Volumes, Free Acid and Total Acid 
Concentrations are Shown, and the 
Statistical Significance of the 
Changes Following Enterectomy 



Con'tcol 

Group A 

P value 

Group B 

P value 

24 hours fed 






* 

Volume ^ 

Free Acid ^ 

111.33 

193.54 

0.05 

185.08 

0.05 

14.26 

26.62 

0,05 

23.96 

N.S . 

Total Acid' 

15.59 

27 .73 

0.05 

25.09 

N.S. 


"k 

Volume in ml. 


Acid in ra.Eq./volume. 


















si-*4 .'-.i' 


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i. ;:!!#' 

" .“is 




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S? 


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iXiirr'i I' ' ••■'l.A' 'S'-'iV . U '=^- 

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>, 3<‘£j j ■*.« ••'■ 1 ‘ . '• JEfioi-• 

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. ;w jr*l ftfte/Jv'V 


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48 


In the fasting state, only Group A showed a greater volume of 
gastric juice than the controls, of 66% (Table 2), In Group B, the 
volume v/as unchanged as compared with the controls, though the acidity 
was almost doubled (Figure 5). None of these changes was statistically 
significant (Tables 13 and 14). 

The effect of feeding was to increase the secretions of all 
dogs, including the controls. 

The twenty-'four hour collections were made during the weekends, 
when activities in the animal house were at a minimum. The dogs were 
not disturbed except for feeding and exercise, and the only time the 
collecting bags were emptied was at the end of the twenty-four hour 
period. Fewer extraneous stimuli were acting on the dogs during this 
time, a high proportion of which time was spent asleep. These factors 
may account for the relatively high hourly secretion compared with the 
eight hour hourly collections taken during the working week. 

Eight Hour Awake Measurements 

With the animals awake, and therefore subject to numerous ex¬ 
ternal stimuli, no sustained nor significant pattern of Heidenhain 
Pouch secretion was evident. 

When fed. Group A produced slightly less Heidenhain Pouch 
secretion than the controls (Table 15), while Group B showed a 60% rise 
(Table 16). Neither change was statistically significant. In all 
three groups, a steep rise in Heidenhain Pouch secretion occurred 
during that hour that followed feeding (Figures 6 and 7). 




. 


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"■%" .; ■ . , / ' ' ■»' 

fl'Au h. fjk> sfrsii' ? 'i u^i t> ^»mU 


'B 


vdJ i(iiw .N?r^ i’i»)*^ (i 't> ’“I- t’i ■*■ io^ drtfjoot.^'Yfi« 


.taiir.;3ri>f, ! f-fjoi 'v Jico Uttjti .litpi© ;; 


t 


ie:>r!i'if(t:\vrr^titn t>Ajt<KA -iuo?! Jrt'|>l3i,|''» 



t-. 


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it ■.; '■=n t,«ti i.pjfei't vfl 

^ ffoVQ^I “iL 

> aji . 

riX't ■ f »t» vuftl tq ntwrtl , ^ 

ur.in #0J • Ct’?**tt/|f) a -slxjTft' ^(^f, i.d'<*vl tltiSiiass •rfd 

- 

Sim Ji .iiiMiilinisJ- ylX.f-'iI.Jfciin aft’f lafU.^dft . (dX ^JdfiT) H 

fi*y,un:x> fXi •«X7 e ,e^f'o:,tp aeidd ;|j 

• (T &<iti ^ -UKWi ppiairp \ii 


49 


TABLE 2.—Mean Total Fasting Heidenhain Pouch Secretions in 
Control Dogs, Dogs with 55% Proximal Enterectomy 
(Group A), and Dogs with 55% Distal Enterectomy 
(Group B). Volumes, Free Acid and Total Acid 
Concentrations are Shown, and the Statistical 
Significance of the Changes Following 
Enterectomy 



Control 

Group A 

P value 

Group B 

P value 

24 hours fasting 






* 

Volume , 

t 

Free Acid , 
t 

Total Acid 

73,83 

123.45 

N.S . 

73.08 

N.S. 

5.08 

13.15 

N.S . 

9.56 

N.S . 

5.64 

14.35 

N.S. 

10.44 

N.S. 


"k 

Volume in ml. 


'Acid in m.Eq./volume. 


















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Fig. 5.—Comparison of the mean twenty-four hour fasting HeicJenhain Pouch 
tion in control dogs, and enterectomized Group A and Group B dogs. Secretion 
ncreased in Group A, and the free and total acid was increased in both groups, 
of these increments was statistically significant. 





























































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ft 


p 


-P 

PQ 

0 


w 




0 

ft -P 


ft 

0 

(d 



O 

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0) 

U 

p 


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c 


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0 

fd 



(d 


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p 

fH 

< 

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0 

p 


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fd 

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ft X 

o 

0 

0 

to 

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X 

0 

•p 

p 


p 

0 

•p 

c 

0 

•p 

0 

fO 


g 

CP 

cu 


•p 

•p 

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ft 73 

to 


p 



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CO 


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c 

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-p 

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0 

p 



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fd 

»p 

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•p 


p 

p 

p 

c 

■p 

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to 

0 

0 

<u 

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cn 

0 

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p 

•H 

U 


(d 

u 


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p 

<0 

Ip 


to 

ft 

0 

ft 


g 


p 

CO 

0 

Ui 

0 

(d 

u 

(U 

p 


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1 

0 

0) 

• 

1—1 

p 

CP 

v£) 

0 

0 

0 


> 


fd 

• 


(U 

X 

tP 

>1 

g 

o 

-r4 

p 

p 


ft 

0 

rH 

p 


p 

0 

0) 


0) 

> 

jp 


p 


p 


o 

(U 

•p 


<u 

X 

(U 


CO 

p 

2: 
























MEAN 8 HR. AWAKE POST PRANDIAL HEIDENHAIN POUCH SECRETION (2) 



I— 

o 


-T— 

LTv 


“1 

cr> 


nOA/bBOJ) QIDV 33 yd 


LTl 


(■10A/b3LU) aiDV TViOi 


o 


Fig. 7.—Comparison of the mean hourly awake postprandial Heidenhain Pouch 
acid concentrations of control dogs, Group A and Group B dogs. Post enterectomy, 
the acid level of Group A diminished, and that of Group B increased. Neither 
change was statistically significant. 















► 






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■|| 

i 


> 










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r *-* 

, I ■ 


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rr ,/ ,a 

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n g. 



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53 


In the fasting state, the decrease in Heidenhain Pouch secretions 
of both Groups A and B was apparent (Tables 17 and 18) and significant 
(p = 0.05), and the diurnal variation of the gastric secretion of the 
fasting dog is well shown by the control group (Figures 8 and 9). 

In both groups, the dogs secreted more when fed than fasting. 
(Tables 3, 4, 5, and 6), 

Eight hours awake fed secre ti ons .-- The general pattern of 
secretion was similar for the controls and both groups: after the 
baseline secretion was established over the first two hours, there was 
a fourfold rise after feeding for the next two hours, followed by a 
gradual decay over the last four hours of collection. 

One interesting observation on the rate of change of gastric 
secretion; although the controls and both groups were fed in the same 
V7ay, at the same times of day, both the rise and fall in gastric juice 
production from Group B was considerably faster than that of the other 
two groups. The steep increase in Heidenhain Pouch secretion in Group 
B after feeding was matched by a steep decline later, so that the col¬ 
lection at the eighth hour amounted to less than that taken at the first 
hour. This latter phenomenon occurred in three out of four conditions 
of collection in Group B, and never in either of the other groups, which 
rose to a lesser height, and sustained a more gradual decay. 

VJith the dogs awake and fed, the gastric hypersecretion that 
follows massive enterectomy was not observed in Group A, but was present 
in Group B. 

Eight hours awa ke fasting secretions .— The diurnal variation 


of gastric secretion without a food stimulus is shown in this category. 








j,.B.>itirtt>itt ^»t\in XI f.nfrtw) hx-cttttrm^ Rfcw H r,Tifi A 


ll; *■. 


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sa 


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ftifj! •iio<t tv,«ft tio’ JTt: > 'i’’’!' uv ^ ti.c«w noJU a-soda 




?.-Vr» ft.vuHi ,?'.rait'r< tm* Jgtil e./t5 rrv‘CiiN-i ... ^io-aa 


il- v'tf Ijawo.r. Col ,rKi<^f - 'ic') 




r .5 I T n 


Ij 


. inj Ji9«fc!X '''j Ic '1 ‘J ; %iaS^ f llRtri?*ip , 


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W-tiO 






0«rB» ni S*! a-jtov 11^6.’. '< ‘' ^^'»'t‘';T '/ i 

..•-Ty 

- • -»^ • ■ jt- 


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■ • i* ■ -i: • ^ <■ 

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iaii'3 J*-‘■ tii..’’,' suvf f.‘5t .r r.iiv ivo^. rf'iSfjJs dfla 4* no4v'.'-'X 


•ftoiJ lN.’:i> a-^ “to I'O^* w* ft^3 fi.*: • ^■lJl>C aim' ."tuxKl 








iii 


HajLrtyrf »Jli^ ^0 nt U>fi 46 qi.fosrj ia. r:odJk^rtJimi 3 o 


<pc»t 


i4i<fiiiii:»p PftcHr f. Ijtifi ,'-^aapoi e o^ ®f»oa 

■; -4 f'-'> 

iftrtd ^ioi:)» i."'j'W'-^f M-”’ v,^^& mh thl^ i 


{WSW t'> { 4.A qji/O'^J T' ••/^**;»‘J(} S»VJRf;l^ rvoliol 


k>; 


i-’ 

.9 


,ff cj^JO^ic^ «ui, 


coit^^. JAV SklT A > 'tiip;'j>m:Jt»«X it2<^-><t ■3(<aia ■. 


■!, 


■ rU nwcwlu ai faog> aXtJAA^ 5o 






I 

yyiiii 


1 .1 ’ 


/., /f:-A I 

■ 



tr 

LTv 





o — 





I>1 

M >1 


O 

4-J 


U 

O 


(U -P 


u 

o 


0) 

u 


<u u 

W 0) 
0) 


0 ) 0 ) 

e e 

13 :3 


Fig. 8.—Comparison of the mean hourly awake fasting Heidenhain Pouch 
s of control group, Group A and Group B dogs. Post enterectomy, the 
s of both groups decreased significantly (p = 0.05). 


















MEAN 8 HR. AWAKE FASTING HFIDENHAIN POUCH SECRETION (2) 


> 


1.0 • 

0.5 - 


0 


CONTROL PERIOD 

GROUP A (PROXIMAL ENTERECTOMY) 
GROUP B (DISTAL ENTERECTOMY) 



_i 1.0 

o 


> 

S 

E 


E 0.5- 


o 

< 


< 

s 


0 J 



0 


-!- 5 - 1 ^ 

TIME IN HOURS 


Fig. 9.—Comparison of the mean hourly awake Heidenhain Pouch 
acid concentrations in awake and fasting control dogs, Group A and 
Group B dogs. Post enterectomy, in Group A there was a significant 
decrease in the free acid (p = 0.01) and the total acid (p = 0.01) 
and in Group B a significant decrease in the free acid (p = 0.01) 
and the total acid (p = 0.05). 
























II 


i 


I 


¥ 


V 




i 





I 





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< fTlfH 1^ ilMii A VOKif 

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'♦"I 

s; 

l0 ^ 



?-?——T~— i —^ T——3-5 

2«jo.s V, ^/},r 


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ta# A tl^Ui I»j,t h#'.* A I 9f\^‘i^i4k-t2n»oe%a‘J f:i.>A 

ft AA% ®'uj« ’ <ji;# X3 nl . v«>i ♦ siMf.* i»c^ t ifyOxC^ 

ro,*?) * (j|;> 

ih Inf taiif bttm ',XQ,0 • ^|) ttftf al ^mA&%cr%h 

{it.O - q) f-fi-t • iT^ ms ci MMl»?t>Slfc % « ^PtO 4i UiM 

.(It).^ « * 1 ) {>io# •c£9 tM* 


















56 


TABLE 3.--Mean Total Eight Hourly Heidenhain Pouch Secretion in Awake 
Controls and Enterectomized Dogs, Fed and Fasting, and the 
Statistical Significance of the Changes Following 

Enterectomy 



Control 

Group A 

Group B 

Statistical 

significance 

' 

Postprandial 

26.22 ml. 

24.46 ml. N.S. 

41.96 ml. 

N.S. 

iFasting 

25.10 ml. 

16.27 ml. p = 0.05 

14.70 ml. 

p = 0.05 






















; i 




T 







'.ViKVu 
' ~> . -.j tl 


I 

d 




li 


v'lfv 

’"il 


' -'1 
-T' -J T 


. . 


r 


^ *r 1 




r .,•' 

'rf ■ ^. 

•'V . 


t. 





SiiUvV'A .if .* .-Dir fl'"‘i<^ >«• |*?ci? SiTiBIT 


{Jt^WBOJ^PP ' ^1' i ^ t. f‘Si*ii'J >’t ifiiiM? 

' ’ ' ' ' . '/ T>^€<'K.'v ■-5 

: f*A’ 


'55- 


9r.vi '■ !•? / 




::^n 




<7 •■■[i>r *-?• 


r' 


j? 1^- 




.e,it 

Cd.O » 5|[ 


-r •• ‘ 






-J- 


* • * ' S '** ^ 

•I • ‘ ■ •■ ^’i • * ^ 

.IM : n,o V .1,,, \: .A< '--Clif c^I 















57 


TABLE 4.--Mean Hourly Heidenhain Pouch Secretions in Awake Dogs 

Control 


Hours 



1 

2 

3 

4 

5 

6 

7 

8 

Dogs fed at the 

end of 

hour t 

wo 






* 

Volimne ^ 

0.90 

0.99 

4.51 

5.04 

5.37 

3.35 

3.05 

3.02 

Free Acid ^ 

0.047 

0.070 

0.325 

0.499 

0.43 2 

0.423 

0.296 

0.252 

Total Acid 

0.051 

0.073 

0.365 

0.537 

0.464 

0.445 

0.323 

0.276 

Dogs fasting throughout 







* 

Volume , 

1.24 

3.14 

4.66 

4.99 

3.64 

2.90 

1.71 

2.82 

T 

Free Acid ^ 

0.083 

0.373 

0.581 

0.573 

0.366 

0.251 

0.126 

0.154 

Total Acid 

0.094 

0.400 

0.619 

0.615 

0.404 

0.283 

0.141 

0.186 


* 

Volixme in ml. 


^Acid in m.Eq./vol. 




























' Ik 1 




I ‘‘is 


-" y ' 

.‘f 



mm 


\ -v ..V 

'.^1 



*i. 


■'i 


*p,xj sr.<fe.^i* . xii 4i I'fi4rauit*»l-2 rf-vjft'l »«• ft/f' P!B-'>'--.A ffJSAT ij 


c 

i A 

.at 


; ^ .• 

,, T. ,^,.. 

’ * 




- '/ 

y_ ( 

■c-'- , 


■ 5 : 0.1 

to.e 

.^1 r 

se’i .0 


ft. 

ats.o 


1 « 

t 


,cv.i 

rsf A 

^^i.0 

ecf .»> 

; .:A' , 

&ai.o 

iA’x.ti 

f. 


1 


”.- ' r!cnr—rv^trx; • .-x-:. 

M>a _ 

♦ 41 (to-* *» 

'S;>kAb.| r 


» ’• 


T " 


\ 

«5t I 

(if 

tr.^' ' ho.?. 




’ * ' ' 
ofvl, \; .■.< V«i ft- ^«i5 ep>oaV' 

— - - -‘v,'. i/S 


'* „■ '•'j ■■'■> 

p.' .<•» 1 




':> , >* 


>■ I 


c:,> U-'t.CI [ omtfloY 


#’■1 


► » 1’ . j ) T » » • W”** - T' p ^ m^n *tw^ 

frf ;.0' V ^ f P ,)>♦' 0 j ■ e S‘iJr-rlV 1^1 tioA 


. 1. 


"I 


a{ >m:.n 


■^r 




'ii 


t: 


I *^l».^ I »*.<,.>•; ‘■AS.i j, 

o' >0 '6'iT t \%jn :if.ni /?, 


arej-foV 

hin^A 




t .'.i . , A 


i_■.'..._'i_.;„,.!i:_ ^ 


'."'f 






.Xjn ni •flwXoV 


*j 


j -t. 


t 


• »( 


t.. 








’ J 

4i 


\ 


. T V t 








il^i.-. t 





■% 



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J. ' 

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58 


TABLE 5.—Mean Hourly Heidenhain Pouch Secretions in Awake Dogs 

Group A (Proximal Enterectomy) 


Hours 

1 

2 

3 

4 

5 

6 


8 

s .S.^ 

Dogs fed at the end of hour 2 







"k 

Volume 

1.00 

1.90 

5.01 

4.15 

4.41 

2.67 

2.91 

2.41 

N.S . 

Free Acid 

Total Acid 

0.092 

0.158 

0.305 

0.367 

0.329 

0.238 

0.168 

0.162 

N.S . 

0.096 

0.166 

0.343 

0.403 

0.353 

0.263 

0.194 

0.186 

N.S . 

Dogs fasting throughout 








* 

Volume 

1.66 

1.99 

2.34 

2.35 

1.90 

1.71 

1.84 

2.48 

p=0.05 

Free Acid', 
Total Acid 

0.173 

0.184 

0.159 

0.117 

0.029 

0.024 

0.008 

0.009 

p=0.01 

0.178 

0,198 

0.175 

0.129 

0.040 

0,036 

0.020 

0.018 
_I 

p=0.01 


Volume in ml. 


Acid in m.Eq./yol. 
t . . . . , 

Statistical significance of the volume and acid concentrations compared 
with the controls. 
























V 







’iSj'i 










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iD" 


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a ‘r «** '' 1 ^ ' 


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4J 


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^ i ^ 


* 5. K ; r> t, CT ■ Is -.t E a cec. .0 ‘- ^»r, h au c. v^oei'-d^X.0 

*--' -- - '“ ^,ii-4.o|AaX.o 


1-- -'\ 

.B^V ' e> #X . 0-'t' * ..-J ! C U**, 0 

i S 1* K 


c 5MOfi[ *^0 B^a 



^6.? 40.1 


L. ;1 


. t • 


Ov. X ! *,. 


fcuoA 

deOid j &JioA 



. . . ' ^ .*-i>' 

'ai}t>^*oni<i ^t,U0B5 'ap6G 


>t.'‘^.J.4.V,.( ^ : 


r - 

SWJIEjIoV 


£04f)-<' ftfr.rv. >is,i' xt»i . . #-x.. •.)I ‘ u 

itt.o-rt t-. t>. <> ♦'Hitt',*j; > .>,:■, '4 f ^; 14’C> [ X.' * • i. c\: "% 

*'*'' ‘ <1* O.C) ^^.J;.0 , ."t‘1'^VX.O ’ bir>A ItJeT ^ 

■’ M_-l_L—!_L.„:L_±.J—I 


U 7 


u 


i(fi nt «r?wXoy. 




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wJov\,jp:^.rt oi bioA 



:j 


half, i' tO jinoli'PTIxr'f. ^ £s. JW^'.^SnV' 5o ftv'Stiii^i/it'ia 


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V 


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;, - s 


*«»-' 





I 

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= i? J 


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r; 

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59 


TABLE 6.—Mean Hourly Heidenhain Pouch Secretions in Awake Dogs 

Group B (Distal Enterectomy) 


Hours 

1 

2 

3 

4 

5 

6 

7 

8 

S .S 

Dogs fed at the end of hour 2 







* 

Volume 

t 

Free Acid , 
T 

Total Acid 

' 

3.56 

6.61 

11.00 

8.65 

4.87 

3.74 

1.74 

1.79 

N.S. 

0.394 

0.754 

1.201 

1.256 

0.624 

0.371 

0.131 

0.147 

N.S. 

1—1 

o 

0.795 

1.275 

1.316 

0.691 

0.404 

0.156 

0.186 

N.S . 

Dogs fasting throughout 








•k 

Volume , 

t 

Free Acid , 
t 

Total Acid 

1.67 

1.92 

1.86 

2.29 

2.41 

1.37 

1.83 

1.35 

p=0.05 

0.149 

0.138 

0.138 

0.133 

0.135 

0.025 

0.042 

0.018 

p=0.01 

0.164 

0.157 

0.155 

0.149 

0.156 

0.035 

0.081 

0.031 

p=0.05 


ic 

Volume in ml. 


"^Acid in m.Eq./vol. 

"^Statistical significance of the volume and acid concentrations compared 
with the controls. 

























It 






,8 ^ 






il) . rjair. 




P» 


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• • Vi — I i— 

r i' f '! i 

11 ^! i “‘t' V, c ^. ’ fci^ J 


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Vi i , 


\r 


I , %i 


^'•1 .o'**'*^ Up4 fc; 


?e. r' tr.] rt. j j i-"./- 

:• i. ] \ : .'i 

i _ 


tr.] 


I 


f.; 

I. 




.<71 

i ui 



:'p<^ T fixiitoA vi'jijoil nr.sH**-..d 


•nV idJaiO^ a > 


tlii.nl 5<? 4>ni 1* fi5l » 


T'V , Ci ’V'<?■ *?{ CN'-; •- , j „ QtniloV . 

;‘f, 0,1'tfl’. ■'' '' , i'i!;«v,'j‘ .0 1' inior ' * 


* 


^<'U^ £?,l| rd.l 
f!.-! .-'1 .tirt. ^'rti/.o 


a; TeCtijj >1.0 

i 


^ ■•.«.< !ov 

^ f ivi\ M' r^ ■ ,v 


LictA 


>!fc 






' .'TW^ 


i* 




' . Tnj ^ t idtiuilciV ^ 
. l<jv\, pfi? ni 


Eooiii'.^inaofivS f fv •» «*.:i;) 'o<7 ;>i.M 3tT3 j 

'■T- -? '-■ * .aJTo’lLtno^ rtti ■ ' 





aJTo’it^no^ »aLi rfliw 

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60 


The rise occurred a little later in Group B (during the fourth and fifth 
hour), than in the controls and Group A (during the third and fourth 
hour). Once again in Group B, the secretion during the final hour of 
collection was less than during the first hour, while in both controls 
and Group A, it remained greater. 

In neither Group A nor B was a hypersecretion demonstrated in 
the fasting collections; on the contrary, both groups secreted sub¬ 
stantially less than before their enterectomies. On the basis of this 
observation alone, it would appear that food is a necessary ingredient 
to stimulate gastric hypersecretion following enterectomy. 

Eight Hour Anaesthetized Measurements 

With the animals anaesthetized, a difference was noted between 
the two groups. 

Group A secreted less than the controls, both in the fed and 
fasting state (Figures 10 and 12); the decrease in volume of gastric 
juice was small and not statistically significant (Tables 7, 8, and 9), 
but there was an important decrease in its acidity (p = 0.05), 

(Tables 19 and 21) . 

Group B, on the other hand, produced an increased secretion over 
the controls (Tables 8 and 10), In the fed state, both volume and acid 
were significantly increased (p = 0.05) (Table 20), (Figure 10 and 11), 
while in the fasting state, the increments were smaller and not 
statistically significant (Figures 12 and 13) (Table 22), 

In the fasting state, the diurnal rise in Heidenhain Pouch 
secretion was seen to occur earlier (second and third hours) than when 
the dogs were awake (third and fourth hours). 


r»fiL U'<ifrf^y'' ni 3fiJ'«*i fil:J#iX 2b«inijooo aiil? «»f{T 



ri-t-Jif .*"' ^tr tn.hij ^yout' fcrj* cft5 nl ;*mi:i t (noofi 

* - P i I 

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, Vr^j'-s-a -xp iX iA q'jc?i0 Nib 

’•' ■ * , 

ni lt'•.l I''t *1 ‘iOTi A rymiD nJ 


»,.•»« fr/iTik^ip .-if-K; p, .t., tiw ji+i.'oi -art:}.' 

•; ^ ' / ^ 'W ’-yj 

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-•* ■ -'' aujim V, 







MEAN 8 HR. ANAESTHETISED POST PRANDIAL HEIDENHAIN POUCH SECRETION 



Fig. 10.—Comparison of the mean hourly anaesthetized post¬ 
prandial Heidenhain Pouch secretory volumes of control dogs, 

Group A and Group B dogs. Enterectomy had no significant effect 
on that of Group A, but significantly increased that of Group B 
(p = 0.05). 







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Q va<'>fo SO if^r * -ti9ni Y'-’ •^* ’■ x/fVi* ‘A »x*^-iC io oo, 












MEAN 8 HR. ANAESTHETISED POST PRANDIAL HEIDENHAIN POUCH SECRETION (2) 


CONTROL PERIOD 

GROUP A (PROXIMAL ENTERECTOMY) 
GROUP B (DISTAL ENTERECTOMY) 



^ » I 1 ■ I I I 

0 1 2 3 4 5 6 7 8 

TIME IN HOURS 


Fig, 11.—Comparison of the mean hourly anaesthetized post¬ 
prandial Heidenhain Pouch acid concentrations of control dogs, 

Group A and Group B dogs. Enterectomy significantly decreased the 
free and total acid concentration in Group A (p = 0.05), and 
significantly increased the free and total acid in Group B (p = 0.05) 












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MEAN 8 HR. ANAESTHETISED FASTING HEIDENHAIN POUCH SECRETION 

- CONTROL PERIOD 

-- GROUP A 

GROUP B 





r oo 




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Fig. 12. Comparison of the mean hourly anaesthetized fasting Heidenhain Pouch 
ory volumes of control dogs, Group A and Group B dogs. No significant changes 
ed following enterectcxny. 























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Fig. 13.—Conparison of the mean hourly anaesthetized fasting Heidenhain Pouch 
acid concentrations of control dogs, Group A, and Group B dogs. Enterectomy 
produced a significant fall in free and total acid concentration in Group A (p = 0.0 
but no significant change in Group B dogs. 


































65 


TABLE 7.—Mean Total Eight Hourly Heidenhain Pouch Secretions in 
Anaesthetized Controls and Enterectomized Dogs, 
Postprandial and Fasting, and the Statistical 
Significance of the Changes Following 
Enterectomy 



Control 

Group A 

Group B 

i "k 

Postprandial volume 

32.62 

30.12 

(N. S .) 

55,21 (p=0.05) 

Fasting volume 

14,40 

13,58 

CN, S .) 

19.70 (N.S.) 


* 

Volume in ml. 




















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66 


TABLE 8.--Mean Hourly Heidenhain Pouch Secretions in Anaesthetized Dogs 

Controls 


Hours 



1 1 

2 

3 

4 

5 

6 

7 

8 

Dogs fed at the 

■k 

Volume ^ 

end of 

1.03 

hour t 

1.55 

wo 

3.91 

7.18 

6.86 

5.53 

3.85 

2.72 

Free Acid ^ 
Total Acid 

0.100 

0.305 

0.433 

0.748 

0.782 

0.710 

0.446 

0.280 

0.124 

0.326 

0.461 

0.797 

0.800 

0.763 

0.474 

0.303 

Dogs fasting th 

* 

Volume ^ 

Free Acid ^ 
Total Acid 

roughoui 

0.09 

t 

0.69 

1.99 

2.39 

2.60 

2.65 

1.86 

2.16 

0.000 

0.042 

0.176 

0.186 

0.156 

0.156 

0.082 

0.200 

0.000 

0.050 

0.192 

0.197 

0.173 

0.176 

0.095 

0.222 


"k 

Volume in ml. 


Acid in m.Eq./vol. 
























rlA. 








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67 


TABLE 9.--Mean Hourly Heidenhain Pouch Secretions in Anaesthetized 

Dogs Group A (Proximal Enterectomy) 


Hours 

1 

2 

3 

4 

5 

6 

7 

8 

S .S 

Dogs fed at the end c 

)f hour 2 







■k 

Volume 

Free Acid . 

0.99 

1.24 

5.91 

6.38 

4.29 

6.29 

2.64 

2.38 

N.S . 

0.110 

0.079 

0.388 

0.797 

0.645 

0.676 

0.244 

0.176 

p=0.05 

Total Acid' 

0.144 

0.093 

0.443 

0.809 

0.681 

0.716 

0.265 

0.195 

p=0.05 

Dogs fasting throughout 








* 

Volume 

• -,t 

Free Acid 
Total Acid 

0.92 

0.94 

2.14 

2,40 

1.86 

1.76 

1.65 

1.91 

N.S . 

0.045 

0.058 

0.128 

0.068 

10.033 

0.048 

0.017 

0.038 

p=0.05 

0.052 

0.067 

0.144 

jo.103 

10.067 

_ 

0.074 

0.030 

0.052 

j p=0,05 


"k 

Volume in ml. 


Acid in m'.Eq./vol. 

"^Statistical significance of voliame and acid concentrations compared 
with controls. 
































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68 


TABLE 10.—Mean Hourly Heidenhain Pouch Secretions in Anaesthetized 

Dogs Group B. (Distal Enterectomy) 


Hours 

1 

2 

3 

4 

5 

6 

7 

8 

S .S .t 

Dogs fed at the 

2 end of hour 2 







* 

Volume 

2.32 

1 

4.67 

8.43 

14,57 

8.08 

9.91 

3.55 

3.69 

p=0.05 

■ 

Free Acid , 

0.383 

0.598 

1.099 

1.943 

1.001 

1.348 

0.433 

0.390 

p=0.05 

t 

Total Acid 

0.396 

0.617 

1,132 

1.991 

1.036 

1.354 

0.448 

0.455 

p=0.05 

Dogs fasting throughout 








* 

Volume , 

1.64 

1.73 

3.80 

3.33 

2.32 

2.72 

2.66 

1.50 

N.S . 

, t 

Free Acid . 

0.044 

0.139 

0.436 

0.351 

0.118 

0.178 

0.156 

0.079 

N.S . 

T 

Total Acid 

0.052 

! 

J__ 

0.154 

0.456 

1 

0.372 

0.145 

0.194 

0.175 

0.083 

N.S . 


Volume in ml. 
i 

Acid in m.Eq./vol., 


^Statistical significance of volume and acid concentrations compared 
with controls. 




























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69 


Eight hours anaesthetized fed secretions .— The sum of the 
means in this category were; 33 ml. for the controls; 30 ml. for 
Group A; and 55 ml. for Group B (Table 10), 

There is a similarity in the pattern of these secretions and 
that of the awake and fed animals. Group A secreted less than the 
control dogs, but Group B produced a significant acid hypersecretion 
(p = 0.05) (Figures 10 and 11). 

Eight hours anaesthetized fasting secretions ,— The sum of the 
means in this category were: 14 ml. for the controls; 14 ml, for 
Group A; and 20 ml, for Group B (Table 10). 

The volume of Heidenhain Pouch secretion in this category was 
less than in any other, suggesting that either the anaesthetic exerts 
a depressor effect on gastric secretion, or that external stimuli apart 
from food may act to increase gastric secretion. 

As in the majority of the eight hour secretions, Group A 
secreted less than the controls, while Group B hypersecreted, Neither 
change in volume was statistically significant, but the decreased 
acidity in Group A was significant (p = 0.05). 

H• Second Stage 

In the second stage of the experiment, the thoracic duct 
lyxaph was diverted in Group A and B dogs, and subsequently reinfused 
intravenously. Heidenhain Pouch secretions v/ere measured hourly for 
eight hours. During the first tv/o hours, baseline Heidenhain Pouch 
secretions from the anaesthetized and thoracotomized dogs were collected; 
over the next four hours, those from the fed animal with the thoracic 
duct lymph diverted were collected; and during the last two hours, the 









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70 


hourly collections were from the dog while the diverted lymph was being 
reinfused into a systemic vein. 

Group A 

The mean baseline Heidenhain Pouch secretions for the anaes¬ 
thetized and thoracotomized Group A dogs was lower than that for 
Group B, and no significant change occurred on diverting the thoracic 
duct lymph and feeding them. Although the Heidenhain Pouch secretions 
were minimal during this four hour postprandial period, it is inter¬ 
esting that virtually no acid was produced in it (Figures 14 and 15). 
Intravenous reinfusion of the lymph, however, produced a highly signi¬ 
ficant increase in their Heidenhain Pouch secretion in every case 
(p < 0.01), (Figure 16), (Tables 23 and 25), 

Group B 

In Group B, the baseline Heidenhain Pouch secretion of the 
anaesthetized and thoracotomized dogs was approximately doubt that of 
Group A (Figure 14) , but no significant change was produced either by 
feeding the dogs and diverting the lymph, nor by reinfusing the lymph 
intravenously (Figure 17) , (Tables 24 and 26). 

General 

The anaesthetized dogs with a thoracotomy secreted less from 
their Heidenhain Pouches than those with closed chests. The baselines 

are therefore lower in this category. 

The expected rise in Heidenhain Pouch secretion after feeding 
the dogs did not occur in Group A, and was seen only rudimentarily in 


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MEAN 8 HR. ANAESTHETISED POST PRANDIAL HEIDENHAIN POUCH SECRETION BEFORE & ARER T. D. 

■-.GROUP A (PROXIMAL ENTERECTOMY) DIVERSION 

. — »GROUP B (DISTAL ENTERECTOMY) 

1 -FEEDING, THORACIC DUCT DIVERTED 



W C 

Q) O 

i C -H 
SOW 


Fig, 14 .—Comparison of the mean hourly Heidenhain Pouch secretory vol 
of anaesthetized and thoracotcanized Group A and B dogs. Feeding and diversi 
of the thoracic duct lymph had no measurable effect on either group. Reinfu 
of diverted lymph significantly increased the secretory volume (p = 0.01) of 
Group A dogs, but had no significant effect on that of Group B dogs. 














MEAN 8 HR. ANAESTHETISED POST PRANDIAL HEIDENHAIN POUCH SECRETION BEFORE & AFTER T. D. 

ai5 


o 

> 

jaio 


QC 


GROUP A (PROXIMAL ENTEREQOMY) 


DIVERSION 


( 2 ) 




Fig. 15.—Comparison of the mean hourly Heidenhain Pouch acid 
concentrations in anaesthetized and thoracotomized Group A and B 
dogs. Feeding and diversion of thoracic duct lymph had no measurable 
effect in either group. Reinfusion of diverted lymph significantly 
increased the free and total acid concentration (p = 0.01) in Group A, 
but had no significant effect in Group B. 













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VOLUME 

IN 

ml. 


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HEIDENHAIN POUCH SECRETION IN DOGS WITH PROXIMAL 
ENTERECTOMY 


HOURS 1 

ANAESTHETIZED 

THORACOTOMiSEO 


nn 

4 L 




THORACIC DUCT LYMPH DIVERTED 






LYMPH REINFUSED 


Fig. 16.—Hourly Heidenhain Pouch secretory volumes in anaes¬ 
thetized and thoracotomized Group A dogs. Mean volumes for the two 
hour fasting, four hour postprandial lymph diverted, and two hour 
lymph reinfusion periods are illustrated with a dotted line. 

























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HEIDENHAIN POUCH SECRETION IN DOGS WITH DISTAL ENTEREaOMY 



o 


Fig. 17.—Hourly Heidenhain Pouch secretory volumes in anaesthetized and 
thoracotomized Group B dogs. Mean volumes for the two hour fasting, four hour 
postprandial lymph diverted and two hour lymph reinfusion periods are illustrated 
with a dotted line. 




































H£ti»iHyw bpocH ZECmioi iM Doe^ oi2iyrBttiBEaowA 

























75 


Group B, This phenomenon, and the simultaneous diversion of the 
thoracic duct lymph, are illustrated schematically in Figure 18. There 
was no significant difference in the amount of thoracic duct lymph 
collected from both groups. 

There was a statistically significant difference (p = 0.05) 
between the Heidenhain Pouch secretions in Groups A and B during the 
first six hours of collection, when those of Group B were greater, and 
a similar statistical difference between the two groups during the last 
two hours of collection, when those of Group A were greater (Tables 27 


and 28) . 




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COMPARISON OF AVERAGE HEIDENHAIN POUCH SECRETION 
AHER THORACIC DUa DIVERSION IN DOGS WITH PROXIMAL 
& DISTAL ENTERECTOMY 


VOLUME 

IN 

ml. 


2 


ANAESTHETIZED THORACIC DUa LYMPH DIVERSION 
THORACOTOMISED 


LYMPH REINFUSION 


DISTAL ENTEREaOMY 

I 

J 


PROXIMAL ENTEREaOMY 


HOURS 1 2 



T 

5 



T 

8 


Fig. 18.—Comparison of mean Heidenhain Pouch secretory volume 
in anaesthetized and thoracotomized Group A and B dogs for the two 
hour fasting, four hour postprandial lymph diverted, and two hour 
lymph reinfusion periods. 

















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1 

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77 


TABLE 11.—Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



Proximal Enterectomy 

% Difference 

Standard 

deviation 

P value 

Significance 

24 hours fed 





Volume 

1.49 

36.554 

2.249 

5 % 

Free Acid 

1,69 

5,762 

2.146 

5 % 

Total Acid 

1.55 

5.857 

2.073 

5 % 
























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78 


TABLE 12.--Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



" ■ • ■ ■ — .. .. - - -- - ■ 

Distal Enterectomy 

% Difference 

Standard 

deviation 

P value 

Significance 

24 hours fed 





Volume 

1,41 

33.438 

2.206 

5 % 

Free Acid 

1.44 

5.374 

1.805 

N.S . 

Total Acid 

1.32 

5.502 

1,728 

N.S . 




















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79 


TABLE 13.—Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



Proximal Enterectomy 

' 

% Difference 

Standard 

deviation 

P value 

Significance 

1 

24 hours not fed 




Volume 

1.85 

30.517 

1.626 

N.S , 

Free Acid 

3.42 

4.383 

1.84 

N.S. 

Total Acid 

3.36 

4.747 

1.836 

N.S . 


























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80 


TABLE 14.--Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



Distal Enterectomy 

% Difference 

Standard 

deviation 

P value 

Significance 

24 hours not fed 




Volume 

0.04 

19.906 

0.038 

N.S, 

Free Acid 

2.39 

3,087 

1.451 

N.S, 

Total Acid 

2.33 

3.168 ■ 

1.516 

N.S. 




















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81 


TABLE 15.--Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



Proximal Enterectomy j 

% Difference 

Standard 

deviation 

P value 

1 

Significance j 

1 

1 

8 hours awake fed 




Volume 

6.96 

0.683 

0.914 

N.S . 

Free Acid 

25.15 

0.094 

1.962 

N.S , 

Total Acid 

23,28 

0.096 

1.942 

N.S . 


















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82 


TABLE 16.—Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



Distal Enterectomy 

o ! Standard 

% Difference | 

i deviation 

P value 

Significance 

8 hours awake f 

Volume 

Free Acid 

Total Acid 

■. —— ■ ■■ .— 

ed 

46.16 

70.21 

67,91 

3.085 

0.414 

0.43 

1.804 

2.163 

2.141 

N.S . 

N.S . 

N.S, 





























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83 


TABLE 17.—Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



Proximal Enterectomy 

% Difference 

Standard 

deviation 

' 

P value 

Significance 

! 

8 hours awake not fed 




Volume 

42.74 

1.113 

2.808 

5 % 

Free Acid 

112.38 

0.178 

3.578 

1 % 

Total Acid 

110.23 

0.187 

3.693 

1 % 


























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84 


TABLE 18.—Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



Distal Enterectomy 

% Difference 

Standard 

deviation 

P value 

Significance 

8 hours av;ake n 

ot fed 




Volume 

52.27 

1.155 

3.185 

5 % 

Free Acid 

105.23 

0.171 

3.57 

1 % 

Total Acid 

98.86 

0.184 

3.491 

5 % 






















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85 


TABLE 19.—Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



Proximal Enterectomy 

% Difference 

Standard 

deviation 

P value 

1 

Significance! 

8 hours asleep 

fed 




Volume 

7.99 

1.347 

0.658 

N.S . 

Free Acid 

19.47 

0.101 

2,365 

5 % 

Total Acid 

20.29 

0.09 

2,917 

5 % 

! 





















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86 


TABLE 20.--Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 


Distal Enterectomy 



% Difference 

Standard 

deviation 

. 

P value 

Significance | 

8 hours asleep 

fed 




Volume 

51.44 

2.516 

3.175 

5 % 

Free Acid 

62.51 

0.384 

3,186 

5 % 

Total Acid 

58.1 

0.391 

2.995 

5 % 





















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— I »— V - t-f-- _ < ^lPii< ' . H ^■||—in>il. "^..^il^. fw. 

•• * • - - • . •^l * 




1 

1 

' ■ 1 

/ e 

1 

K’Vl.f, 


«)<• f . f 

. ‘ it g- 

1 



.. ~ 1.. ..-il..* J 


be>^ qu»Iu» evijvd 8 


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/ 


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I ^bto/T ao’i3^ 
bicA r^fpT 






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87 


TABLE 21.--Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 



Proximal Enterectomy | 

1 

% Difference 

Standard 

deviation 

P value 

Significance! 

1 

8 hours asleep 

not fed 



j 

Volume 

5.92 

0.552 

0.531 

N.S. 

Free Acid 

79.03 

0.072 

2.787 

5 % 

Total Acid 

61.08 

0.071 

2.563 

5 % 


















..... . • ^ t 





l.=V'- -' V« 



« 

.*>1 




T’ 


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1 • t f 


.' i i t 


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, > (V * ' 


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in <,»«'' ’tfiTvi*/ Rn0i.5p iot>8 1 . 


. 1 


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trjtiA 





























88 


TABLE 22.—Statistical Analysis Comparing Mean Heidenhain Pouch 

Secretions Under the Various Conditions of 
Collection with Control Figures 


Distal Enterectomy 



% Difference 

Standard 

deviation 

. . . 

P value 

Significance 

8 hours asleep 

not fed 




Volume 

30.95 

0.876 

2.131 

N.S . 

Free Acid 

40.12 

0.117 

1.511 

N.S . 

Total Acid 

38.36 

0.123 

1.505 

N.S . 




















4 







•* . *• 


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89 


TABLE 23.—Hourly Heidenhain Pouch Secretion in Group A Dogs During 
Baseline Collections (Hours One and Two ), Postprandial 
Collections with Thoracic Duct Lymph Diverted (Hours 
Three, Four, Five and Six), and Post Lymph. Rein¬ 
fusion Collections (Hours Seven and Eight); and 
Mean Hourly Volimues and Acid Concentrations 


Hours 


( 

1 ! 

2 

3 1 

4 

5 

6 

7 

8 

Number of Dog 









F 622 

0 

0 

0 

0 

0 

0 

2.5 

3.0 

F 307 

0 

0 

0 

0 

0 

2.5 

11.0 

10.0 

F 678 

0.3 

0.1 

1 — t 

• 

o 

0.1 

0 

0 

2.5 

1.0 

F 740 

0.1 

0.3 

0 

0 

0 

0 

3,0 

2.0 

F 1232 

0.1 

1.5 

0.1 

0 

0.4 

0.3 

3.0 

2.5 

F 564 

0.1 

1.5 

0.6 

1.5 

1.5 

1—I 

• 

r—1 

1.4 

2.0 

Means 









* 

Volume 

0.1 

0.6 

0.1 

0.3 

0.3 

0.6 

3.9 

3.4 

Free Acid , 

0.000 

0.000 

0.000 

0.000 

0.000 

0.000 

0.078 

0.120 

Total Acid' 

0.002 

0.002 

0.001 

0.000 

0.000 

i 

0.000 

0.105 

0.141 


* 

Volume in ml. 


^Acid in m.Eq./vol. 

































Ph 


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90 


TABLE 24.—Individual Hourly Heidenhain Pouch Secretion in Group B 
Dogs During Baseline Collections (Hours One and Two), 
Postprandial Collections with Thoracic Duct Lymph 
Diverted (Hours Three, Four, Five, and Six), 
and Post Lymph. Reinfusion Collections 
(Hours Seven and Eight); and Mean 
Hourly Volumes and Acid 
Concentrations 


Hours 



1 

2 ! 

3 

4 1 

5 i 

6 

7 

8 

Number of Dog 

F 303 

0 

0 

0.2 

0 

0.3 

0.2 

0.4 

0.5 

F 306 

2 

0.1 

0 

0.1 

0.6 

1.0 

0.8 

0.7 

F 357 

2 

0.1 

0.2 

0.3 

0.1 

3 

0.1 

0.1 

F 335 

0.1 

1.5 

1.2 

1.2 

1 

2 

1.4 

2.0 

F 550 

0.3 

0.4 

3.5 

1.2 

2 

1.4 

1.5 

2.0 

F 1040 

0 

0.1 

0.4 

0.4 

0.1 

0.3 

0.3 

0.8 

Means 









■k 

Volume ^ 

Free Acid ^ 

0.7 

0.4 

0.9 

0.6 

0,7 

1.3 

0.8 

1.0 

0.032 

0.002 

0.008 

0.003 

0.010 

0.025 

0.010 

0,005 

Total Acid 

0.037 

0.003 

0.012 

0.004 

0.013 

0.032 

0.013 

. - . 

0.007 


Volume in ml. 


^Acid in m.Eq./vol. 































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91 


TABLE 


25.—Comparison of Hours Seven and Eight with 
of Secretion in the Thoracic Duct 
Proximal Enterectomy 


the. First 
Diversion 


Six Hours 
in 



% Difference 

Standard 

deviation 

P value 

Significance 

Volume 

35.5 

■ ' 

0.245 

13.576 

1 % 

Free Acid 

50 

0.014 

7,14 

1 % 

Total Acid 

48.67 

0.012 

10.348 

1 % 























le 


•€l -v.fl 

■■ k'V' 
» * , 


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J'iP'f »«>*'* -- 














92 


TABLE 26.—Comparison of Hours Seven and Eight with the First Six Hours 

of Secretion in the Thoracic Duct Diversion in 
Distal Enterectomy 



% Difference 

Standard 

deviation 

P value 

Significance 

Volume 

2 

0.286 

0.442 

N.S . 

Free Acid 

6.14 

0.01 

0.577 

N.S . 

Total Acid 

5.62 

0.012 

0.577 

N.S . 



















.i 





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93 


TABLE '2n Ms3.n of ths Fiirst Six Houirs of ths Thoiracic Duct Divsirsion 
in Dogs with Distal Enterectomy Compared with the Mean 
of the First Six Hours of Duct Diversion in Dogs 
with Proximal Enterectomy 



% Difference 

Standard 

deviation 

P value 

Significance 

1 

1 

j Volume 

76.3 

0.363 

2.82 

5 % 

! Free Acid 

200 

0.012 

2,677 

5 % 

Total Acid 

181.07 

0.014 

2,767 

5 % 























i' V j-!i 

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• \ ^ T-' 

. -.1 Tjp 






If 




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■ 

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mm. 


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94 


TABLE 28.—Mean of the Last Tvvo Hours of the Thoracic Duct Diversion 
in Dogs with Distal Enterectomy Compared to the Last 
Two Hours of the Proximal Duct Diversion 



% Difference 

Standard 

deviation 

i 

P value 

i 

Significance 

Volume 

30.55 

1 0.39 

7,109 

5 % 

Free Acid 

42.97 

1 0.03 

3.089 

N.S, 

Total Acid 

42,48 

j 0.025 

4.444 

5 % 















I 


4 








t t 





6 





1 . 

t 


.<■ 








> 


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I .■;. 


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r 'M 


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95 


DISCUSSION 

I. Twenty-Four Hour Studies 

The gastric hypersecretion that follows massive enterectomy 
was demonstrated in both Group A and Group B dogs, during the twenty- 
four hour postprandial collections, v/hen significant increases over the 
control secretions were noted. This hypersecretion may be the result 
either of adding a secretogogue, or removing an inhibitor to gastric 
secretion, or both. 

In the twenty-four hour fasting collections, the hypersecretion 
was present in Group A dogs, but not in those of Group B. Since both 
Groups hypersecreted when fed, it is possible that the hypersecretory 
potential remains present in both groups when fasting, but in the case 
of distally enterectomized dogs, requires the additional stimulus of 
intraluminal food to show it, 

II. Eight Hour Studies 

The modest decrease in Heidenhain Pouch secretion after fifty- 
five per cent proximal enterectomy in awake and anaesthetized, fed and 
fasting dogs has not been described before, to the best of the author's 
knowledge. It suggests that either a weak secretogogue was removed with 
the jejunum, or that the influence of an inhibitor to gastric secretion 
is being more strongly felt in the absence of the proximal half of the 


sm.all intestine. 




7 




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WoJi a.i ■ 4^<6bofa oriT 


‘ibf^ll ix^l k f'nf, -'ll XrtntiJKPlSQ 4rt«0*?aq •vi’t J 

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96 


The increased Heidenhain Pouch secretion that occurred in Group 
B dogs in the eight hours awake fed, and eight hours anaesthetized fed 
and fasting categories, may indicate the existence of an ileal inhibitor 
to gastric secretion, or of a jejunal secretogogue. The effect of distal 
enterectomy would be to remove this inhibitor, or permit the jejunal 
secretogogue to act more effectively. The failure of the mean eight 
hour awake fasting samples to show a hypersecretion may be further 
evidence that a food stimulus is needed in awake and fasting dogs with 
a distal enterectomy. A small rise in Heidenhain Pouch secretion was 
seen in distally enterectomized fasting dogs, but only under anaes¬ 
thetized conditions. 

Gastric hypersecretion following enterectomy is an established 
response that has received much attention, and is demonstrated in our 
work in the postprandial eight hour studies on Group B dogs. In the 
Group A (proximally resected) dogs, a gastric hyposecretion was observed. 
This is a phenomenon that has not so far been demonstrated. In order 
to produce a decreased Heidenhain Pouch secretion, the effect of known 
secretogogues such as antral gastrin would have to be overcome. This 
argues in favour of an ileal inhibitor. 

On the other hand, convincing evidence of a secretogogue comes 
from the studies on diversion and reinfusion of thoracic duct lymph. 

With the thoracic duct intact, all anaesthetized dogs who were fed showed 
a steep rise in Heidenhain Pouch secretion within the hour. But the 
dogs that were fed, and whose thoracic duct lyraph simultaneously diverted, 
showed no detectable change in Heidenhain Pouch secretion for the four 




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97 

hours that followed. On reinfusion of the lymph at the end of this 
period, the highly significant rise in Heidenhain Pouch secretion that 
occurred in Group A dogs furnishes good evidence of the presence of a 
lymph borne humoral secretogogue in dogs with a proximal enterectomy. 

Since the time of Pavlov, the ability of the small intestine to 
exert both stimulatory and inhibitory influence on gastric secretion 
has been recognized; but its contribution has been traditionally re¬ 
garded as the least important "phase". As a result of recent post- 
enterectomy studies, the intestinal mechanism is assuming an unsuspected 
significance, and its role in the regulation of gastric secretion is 
undergoing reappraisal. An increase in gastric secretion has been 
shown to be mediated by the intestinal mechanism; the possibility exists 
that with a fuller understanding of the nature of this phenomLenon, a 
decreased gastric acidity may be clinically achievable, with its con¬ 
sequent therapeutic application. 

In addition to our above theories other possible mechanisms of 
gastric hypersecretion following enterectomy are discussed. 

III. Possib le Mechanisms of Gastric Hypersecretion Following Ente rectomy 
Potentiation of Secretogogues 

Prolonged gastric emptying time .— Gastrin is secreted in pro¬ 
portion to the length of time that the antrum is stimulated (1). Some 
authors have reported delayed gastric emptying times following enterec¬ 
tomy (2), while others have questioned it (3, 4, 5). Delayed gastric 
emptying was not a feature of Chov/'s dogs postenterectomy C5) , the 
barium mixture transit time remaining at three hours both before and 


after the resections. 




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98 


Liver damage .— It has been postulated that damage to the liver 
in the course of surgery for enterectomy had resulted in an inability to 
inactivate secretogogues such as histamine(6). Chow (5) detected no 
histological nor biochemical change in canine livers.after massive enter¬ 
ectomy, and pointed out that the hypersecretions he produced were im¬ 
mediate, whereas hepatic cellular degeneration would be a slower, bio¬ 
logical process. 

Infection .— Sepsis has been shown to cause a rise in gastric 
acid production (7), but was not a feature of the postoperative course 
of Chow's animals. 

Corticosteroids .— The adrenocortical response to stress in 
man has been shown to produce a transient gastric hypersecretion (8). 

The stress following a surgical procedure like enterectomy is short 
lived in the dog, but protagonists (9) and antagonists (4) of this view 
as a source of the gastric hypersecretion follov/ing enterectomy may be 
quoted. Chow (5) found that the Heidenhain Pouch secretions were un¬ 
changed after a sham operation in which he transected the bowel and re¬ 
sutured it without resection; and concluded that this was not the 
mechanism of hypersecretion. 

"Intesti nal Phase" .— In the Pavlovian concept, this phase 
occupied the least important position of the three mechanisms. It has, 
however, assumed a new importance after enterectomy, and is the subject 
of this study. 

Traditionally, antral gastrin is implicated in the production 
of acid from the parietal cells, whether by the direct action of the 








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gastric "phase", or the indirect "permissive" action of the vagal 
"phase". Chow (5) has produced a substantial acid hypersecretion in 
the absence of the antrum, by performing a massive enterectomy on 
antrectomized dogs. This may be evidence of a secretogogue from the 
retained intestine acting on a target organ other than the pyloric 
antrum, A gastrin like material has been extracted from the duodenum 
of hogs (10), and it is possible that similar hormones may be present 
throughout the small intestine. The proposed secretogogue may be a 
weak stimulator of gastric secretion, or it may act to potentiate 
gastrin. 

Evidence in favour of this mechanism comes from the studies 
of Yakimets and Bondar (11), and later Chow (5), from experiments in 
thoracic duct lymph diversion. Enterectomized, hypersecreting dogs 
sustained a fall in Heidenhain Pouch secretion when the thoracic duct 
l^miph was diverted to the exterior, but resumed their hypersecretion 
when the lymph was reinfused intravenously. When the saiae procedure 
was performed on enterectomized and antrectomized hypersecreting dogs, 
the drop in secretion occurred on diverting the thoracic duct lymph, 
but there was no resumption of hypersecretion on lymph reinfusion. 

Removal of Inhibitors 

Increase in gastric secretion is now an established clinical 
phenomenon following massive enterectomy, although the mechanism re 
mains obscure. If it were due entirely to the gain of a gastric 
secretogogue, it would not be possible to produce a decreased gastric 
secretion by removing any portion of the small intestine. In the dog 
of Group A in the present experiment, a decreased Heidenhain Pouch 








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secretion was produced in every case in the eight hour collections. 

Secretogogues such as antral gastrin continue to act in the 
experimental dogs. Reinforcement of their action by the gain of 
other secretogogues, strong or weak, following enterectomy might pro¬ 
duce moderate to high levels of gastric juice production. But the 
repeated production of a decrease d secretion (in the eight hour col¬ 
lections) against the known stimuli to gastric secretion, suggests a 
potent inhibitor rather than experimental artifact. 

Inhibitors of gastric secretion derived from the antrum have 
been demonstrated by Menguy (12) and Harrison (13), and Thompson (14), 
have suggested the existence of a chalone. Secretin and Cholecystokinin 
(15, 16, and 17) are both known to exert an inhibitory influence on 
gastric secretion. Bile salts given intravenously have been shown to 
have a similar depressant action (18). In both groups of dogs in the 
present study, the enterectomies left antrum and duodenum intact, so that 
the known inhibitors described above were constant for both groups. 

Other substances have been described which are thought to ori¬ 
ginate in the small intestine, and cause an inhibition of gastric sec¬ 
retion. Enterogastrone, described in 1930 by Kosaka and Lim (19), was 
thought to be liberated from the upper intestine in the presence of fat. 
Subsequently doubted by Gregory (20), the existence of this hormone in 
the substance of the small intestine may be germane to this study. It 
would, however, be necessary to postulate that it acted from the distal 
rather than the proximal small intestine; and the possibility arises that 
a related hormone, or an enterogastrone potentiator, may be implica'ted. 






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A chalone originating in the ileum, corresponding to enterogastrone 
in the jejunum, would furnish a partial explanation of the phenomena 
observed in this study. 

Serotonin has been described as occurring along the whole length 
of the small intestine (21), and its effect on gastric secretion is 
known to be inhibitory (22, 23). Doubt persists as to the exact 
function of Serotonin in the alimentary tract, although intraperitoneal 
injection of it into rats has led to intense vasospasm and eventual 
ulceration (24). This has suggested a possible mode of action for the 
observations by Black (22), and Shay (23), of its inhibitory role in 
both secretion and motility of the digestive tract. Substances shown 
to release Serotonin from the v/all of the small intestine after being 
introduced into the lumen include acid and hypertonic solution (25, 26, 
27). It is possible that after a proximal enterectomy, the relatively 
undigested chyme entering the ileum would be both more acid, and more 
hypertonic than the customary physiological content, and that the 
Serotonin thus released might account for the decreased Heidenhain Pouch 
secretion observed in this study. 

Histaminase, like Histamine, is also widely distributed along 
the length of the small intestine (28). Histamine is a potent stimulator 
of gastric secretion, and it follows that the enzyme antagonizes this 
effect. Grossman has demonstrated this action (29), and Sircus has used 
a Histaminase inhibitor to allow Histamine to work unopposed (30). Chow 
has proposed that after massive small intestinal resection, the secretory 
surface for Histaminase is sufficiently diminished to allow the cir- 


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102 


culating Histamine to exert its full effect on the parietal cells, thus 
producing a gastric hypersecretion. He concedes that no physiological 
role has been established for this enzyme, and cites the work of Blair 
(31), who showed that antihistaminic drugs given systemically have no 
effect on parietal cell output. 

The present study was designed to contrast the effects of 
proximal with distal enterectomy, and to determine whether any dif¬ 
ferences existed, Chow's study had been carried out on dogs with a 
"massive" enterectomy, or dogs with both a proximal and distal resection. 
Would a smaller resection have been sufficient to cause it? Was the 
simultaneous removal of both proximal and distal intestine synergistic 
or antagonistic? Was there a balance of secretogogue and inhibitor 
throughout the small intestine, responsible for the "intestinal phase"? 

Chow's initial fall in Heidenhain Pouch secretion in both groups 
(i.e. enterectomized; and enterectomized and antrectomized) established 
the presence of a secretogogue carried in thoracic duct lymph. The 
absence of a return of hypersecretion in the second group on reinfusion 
of the l^miph indicated that the secretogogue acted to stimulate or 
potentiate the events set in motion by the antral gastrin. In the 
present study, dogs having a proximal enterectomy hypersecreted on re¬ 
infusion of the lymph, but those with a distal resection did not. In 
both of these groups, the antra were intact, suggesting a difference in 
secretogogue production between proximal and distal intestine, and 
rendering a significant contribution from the colon unlikely. 


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103 


A shorter length of intestine was resected in the present study 
than in that of Chow, but a greater hypersecretion was produced. How¬ 
ever, the baseline levels in the enterectomized and thoracotomized dogs 
was low. No steep fall was therefore demonstrable on diverting the 
thoracic duct lymph of the present dogs, the baseline levels being al¬ 
ready minimal. On reinfusion of the lymph, however, those dogs that 
hypersecreted (Group A) reached secretory levels seven times greater 
than their resting level, while Group B exhibited no measurable change. 
Thus, dogs in whom the ileum remains intact after a partial enterectomy 
have a potent stimulus to gastric secretion carried in the thoracic 
duct lymph. Removal of the ileum, and sparing of the jejunum, removes 
this stimulus. 

When the thoracic duct is left intact, the opposite result is 
obtained from the two groups of enterectomized animals. The stimulus 
to hypersecrete when fed occurs in dogs from v/hom the ileum has been 
removed. This observation is in keeping with the data of Osborne in 
1966 (4). It follows, therefore, that a minimum of two mechanisms, one 
stimulatory and the other inhibitory, must be acting to produce these 
conflicting results. 

With the above idea in mind one simple explanation of the ob¬ 
served phenomena is that in addition to the antral secretogogue, a weak 
jejunal secretogogue and a stronger ileal inhibitor are present in the 
dogs intestinal tracts. This inhibitor may be labile, and quickly 
lose its potency outside the body, so that it is ineffective when re¬ 
infused intravenously with the lymph. The thoracic duct is proposed 



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104 


as a transport for the jejunal secretogogue. Thus: 

(i) When a proximal enterectoray is performed, the jejunal 
secretogogue is lost, and the resultant of the antral secretogogue and 
the strong ileal inhibitor is a small fall in Heidenhain Pouch 
secretion. 

(ii) When a distal enterectomy is performed, the ileal inhibitor 
is lost, and the secretogogue(s) act together to raise the pouch 
secretion considerably. 

(iii) When the thoracic duct lymph is diverted and reinfused in 
a proximally enterectaniized dog, both the antral secretogogue and the 
ileal inhibitor are transported in the lymph, but the short lived in¬ 
hibitor may be lost by the end of four hours, when the reinfusion takes 
place, and only the effect of the secretogogue is felt, giving the steep 
rise in Heidenhain Pouch secretion. 

(iv) When the thoracic duct lymph is diverted in a distally 
enterectomized dog, the absence of the ileal inhibitor ensures a higher 
level of baseline Heidenhain Pouch secretion. On reinfusion of this 
lymph, the small rise in Heidenhain Pouch secretion over this relatively 
high baseline level represents the effect of the jejunal and antral 
secretogogues carried in this lymph. 

IV. Conclusions 

The Heidenhain Pouch hypersecretion that follows massive 
enterectomy may be produced mainly by resection-of the distal small 


intestine. 




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105 


Proximal enterectomy produces a mild decrease in Heidenhain 
Pouch secretion. 

Reinfusion of thoracic duct lymph intravenously stimulates a 
twelvefold increase in Heidenhain Pouch secretion in dogs with a proxi¬ 
mal enterectomy. 

Reinfusion of thoracic duct lymph intravenously causes only a 
small rise in Heidenhain Pouch secretion in dogs with a distal enter¬ 
ectomy, but the baseline secretion is at a higher level. 

The existence of a short lived ileal inhibitor to gastric 


secretion is proposed. 


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106 


FOOTNOTES 


GROSSMAN, N.I. Proof of a humoral mechanism for gastric 
secretion. Am. J. Phys,, 153 :1 , 1948. 

2 

STAHLGREN, L.H., UMANA, G., ROY, R., and DONNELLY, J. A 
study of intestinal absorption in dogs following massive small 
intestinal resection and insertion of an antiperistaltic segment. 

Ann. Surg., 156 ;483, 1962. 

3 

LANDOR, J.H., and BAKER, W.K. Gastric hypersecretion 
produced by massive small bowel resection in dogs. J. Surg. Research, 
£:518, 1964. 

4 

OSBORNE, M.P., FREDERICK, P.L., SIZER, J.S., BLAIR, D., 

COLE, P., and THUM, W. Mechanism of gastric hypersecretion following 
massive intestinal resection, clinical and experimental observation. 

Ann. Surg., 164 :622-634, 1966. 

^CHOW, K.Y. Effect of enterectomy on gastric secretion. 

M.Sc. Thesis, University of Alberta, 1968, 

^SILLEN, W., HEIN, M.F., ALBO, R.J., and HARPER, H.A. Influence 
of liver upon canine gastric secretion. Surgery, 29-36, 1963. 

7 

HOWE, C.W., WIGGLESWORTH, W.C., and POWELL, W.J. Gastric 
secretory responses to surgical stress and infection. Surg. Forum, 

3^:34, 1952. 

O 

GRAY, S.J., BENSOM, J.A. Jr., REIFENSTEIN, R.W., and SPIRO, H.M. 
Chronic stress and peptic ulcer. I. Effect of corticotrophin (ACTH) 
and cortisone on gastric secretion. J.A.M.A., 147 ;1529, 1951, 


9 

MOORE, F.D. Metabolic care of the surgical patient. 
Saunders, Philadelphia, 1959. 

^^LAI, K.S. Studies on gastrin. Gut, 5:327, 1964. 









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’ 







107 


11 

YAKIMETS, W.W., and BONDAR, G.F. The effect of complete 
thoracic duct lymph diversion on gastric secretion in dogs. Canad. 

J. Surg., 2^:218-222, 1967. 

12 

MENGUY, R.B., MASTERS, Y.F., and GRYBOSKI, W.A. Isolation 
of a gastric inhibitor substance in canine gastric juice. Surg. Forum 
2^:951, 1963. ' ' 

HARRISON, R.C., LAKEY, W.H., and HYDE, H.A. The production of 
an acid inhibitor by the gastric antrum. Ann. Surg., 144:441, 1956. 


14 

THOMPSON, J.C., TRAMONTANA, J.A., LENNER, J.H., and STALLINGS, 

J.O. Physiologic scope of the antral inhibitory hormone. Ann Surg 
156 :550, 1962. - ‘ 


GILLESPIE, I.E., and GROSSMAN, M.I. Inhibitory effect of 
secretin and cholecystokinin on Heidenhain Pouch responses to gastric 
extract and histamine. Gut, 5:342-345, 1964. 

16 

GREENLEE, H.B., LOUGHI, E.H., GUERRERO, J.D., NELSEN, T.S., 
EL-BEDRI, A.L., and DRAGSTEDT, L.R, Inhibitory effect of pancreatic 
secretion on gastric secretion. Am. J. Physiol., 190 :396, 1957. 


17 

JORDON, P.H., and PETERSON, M.D. Effect of secretin upon 
gastric secretion. Ann. Surg., 156 :914-923, 1962. 


18 

NICOLOFF, D.M. Relationship of bile and gastric secretion. 
Surg. Forum, ^:329, 1966. 

19 

KOSAKA, T., and LIM, R.K.S. Demonstration of the humoral agent 
in fat inhibition of gastric secretion. Proc. Soc. Exp. Biol N v 
27:890-891, 1930. 


GREGORY, R.A. Enterogastrone - a reappraisal of the problem. 
Symposium on Gastric Secretion (Edmonton, Alberta, Canada, September, 
1965). London, The Pergamon Press. 

21 

FELDBERG, W,, and TOH, C.C. Distribution of 5-hydroxy- 
tryptamine (serotonin, enteramine) in the wall of the digestive tract. 
J, Physiol., 119:352, 1953;.. 


22 

BLACK, J.W., FISHER, E.W., and SMITH, A.N. The effects of 5- 
hydroxy-tryptamine on gastric secretion in anesthetized dogs. 

J. Physiol, 141:27, 1958. 








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108 


23 

SHAY, H,, SUN, D.C.H,, and. GRUENSTEIN, M. Action of psy~ 
chopharmacologic agents on interdigestive gastric secretion in the rat. 
Proceedings of the Third World Congress of Gastroenterology, 1958. 
Williams and Wilkins Co., Baltimore, Volume 1, p. 108, 1959. 

24 

TOBE, T., FUJIWARA, M., and MURYOBAYASHI, T, Ulcerogenic 
effect of 5-hydroxytryptamine (serotonin) in the stomach. Ann. Surg. 
]^:1002, 1967. 

25 

RESNICK, R.H., and GRAY, S.J. Chemical and histological demon- 
stration of hydrochloric acid—induced release of serotonin from in¬ 
testinal mucosa. Gastroenterology, 42:48, 1962. 

26 

0 HARA, R.S., FOX, R.O., and COLE, J.W. Serotonin release 
mediated by intraluminal sucrose solutions. Surg. Forum, 10:215, 1959. 

27 

DRAPNAS, T., MCDONALD, J.C., and STEWART, J.D, Serotonin 
release following instillation of hypertonic glucose into the proximal 
intestine. Ann. Surg. 156:528, 1962, 


28 

CODE, C.F. Histamine and gastric secretion. In: Histamine. 
Ciba Foundation Symposium, edited by G.E.W. Wolstenholme and C.M. 
O'Connor. Boston. Little and Brown, 472:189-219, 1956. 


29 

GROSSMAN, M.I., DUTTON, D.F., and IVY, A.C. An attempt to 
prevent histamine-induced ulcers in dogs by administration of entero- 
gastrone extracts. Gastroenterology, 6:145, 1946. 

30 

SIRCUS, W. Effect of Bl-pyridimine on gastric secretion. 
Quart. J. Exp. Physiol., 28:91, 1953. 

31 

BLAIR, D. W., and FORREST, A.P.M. Effect of local anti¬ 
histamines on gastric secretion in dogs. Brit. J. Surg., 47425, 1960. 





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PART 2, EFFECTS OF MASSIVE ENTERECTOMY AND AN ANTIPERISTALTIC SEGMENT 


ON GASTRIC SECRETION 






REVIEW OF THE LITERATURE ON REVERSED INTESTINAL SEGMENTS 


In 1896, the Johns Hopkins Hospital Report published the 
results of an experiment conceived by Mall (1). He had reasoned that 
patients v/ho had undergone massive small intestinal resection would 
derive benefit from reversal of the direction of peristalsis of a 
segment of the remaining bowel. William Halstead (2), his surgical 
colleague, tried the procedure on eleven dogs. Eight of these died 
within a few days from peritonitis, but the remaining three lived for 
eighteen, twenty-five, and sixty-four days respectively. It is re¬ 
corded that the latter two had reversed segments measuring twenty-nine 
centimeters and eighty centimeters, and died of intestinal obstruction. 
As a result of this report, the procedure was condemned as lethal, and 
fell into disfavor. A quarter of a century was to pass before a 
scientific reappraisal of this original idea was undertaken. 

In 1927, Ivy (3), using a variety of different lengths of re¬ 
versed segment, was able to produce what he called a physiological 
partial obstruction in some dogs, and demonstrate that the principle 
was sound. Hammer (4, 5, 6) and his colleagues in Michigan sub¬ 
sequently carried out prolonged investigation in this field in the 
1950's, and enunciated certain rules and criteria as a result of their 
study. They discovered that dogs with two-thirds of the small intestine 
can survJ-ve, but that diarrhea, cachexia and death within 


109 


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ninety days follows removal of eighty per cent or more of the intestine. 
Reversal of about 5 cm. of the distal intestine was found to be ef¬ 
fective in maintaining nutrition and keeping these dogs alive. Less 
successful results attended Hammer's more proximal reversals. The 
dogs in whom he reversed the entire duodenum following massive resection 
survived, the stomach and adjacent duodenum became dilated, and ul¬ 
ceration occurred at the proximal suture line after several months. 

In 1959, Hammer and his associates (7) concluded that 

"animals v/ith 80 - 90% of the small bowel removed survive and 
maintain weight if 1 - 2 inches of the distal segment of re¬ 
maining bowel is reversed, and reinserted into the intestine 
in an anti-peristaltic manner". 

The site of these reversals was the distal ileum. Hammer noted at the 
same time that some human mesenteric thromboses involved 80 - 90% of 
the small intestine, and speculated on the therapeutic application of 
his finding to human patients. 

The problem of whether reversed peristalsis would continue to 
act indefinitely against the stream was investigated by Singleton and 
Rov/e in 1954 (8) . Laparotomies were performed at varying intervals up 
to a year post-reversal, and peristalsis in the original direction was 
consistently observed in the reversed segment. This finding was cor¬ 
roborated in 1962 by Stahlgren et al (9), who recorded the maintenance 
of reversed peristalsis in dogs into whom they had inserted an anti- 
peristaltic segment of small intestine up to a year previously. In 
addition to this original observation, Singleton and Rowe noted that 
the stomach and intestine proximal to the site of the reversed segment 
became dilated, and that this dilatation sometimes extended into the 


reversed segment itself. 




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This dilatation was the result of the "physiological partial 
obstruction" that Ivy had described thirty years earlier. The length 
of the reversed segment determined the degree of obstruction, and the 
aim of the procedure was to achieve the longest antiperistaltic segment 
without producing a complete obstruction. Segments as small as 2.5 cm. 
had been shown not to alter metabolism in the dog. Sake (10) and his 
associates began experimenting with different lengths, and concluded 
that a reversed segment of 7.5 cm. in the jejunum was the optimum length 
in a small dog with a total intestinal length of about 300 cm. They 
found that weight was maintained in dogs with a massive enterectomy 
follov/ed by this reversal, and stomach emptying and transit times were 
delayed for varying periods of time. Stahlgren (9) and his associates 
in 1962, had produced an obstruction in the small intestine of a dog by 
reversing a segment of jejunum five inches long, and subsequently 
relieved it by resecting one-half of the reversed segment. 

Going one stage further, Mackby (11) discovered in 1965 that if 
the reversed segment was combined with a recirculating loop, the meta¬ 
bolism could be further increased in animals with an "optimum" re¬ 
circulating loop. This procedure involved transposition of the entire 
residual segment of small intestine, but instead of a linear reversal, 
the bowel was fashioned into a recirculating loop with a circular motion 
of the contents, and the maximum length of linear antiperistaltic in¬ 
testine (proximal to the loop) was only about 4 cm.—a length Mackby 
found to be optimal with a linear reversal. The distal portion of the 
loop was anastomosed to the remaining portion of the ileirni, permitting 




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escape of the contents into the colon. Dogs with this arrangement have 
regained their preoperative weight and vigor, and produced semi-formed 
stools, while remaining in positive nutritional balance. 

In 1965, there was general agreement that reversal of up to 
7.5 cm. proximally, and up to 12 cm. distally, of small intestine, 

V70uld often serve to compensate for severe loss of absorbing surface (12) . 
But on occasion, anenteric cachexia would supervene even in dogs with 
this "optimal" reversal, and it became apparent that delay transit in 
some instances could not entirely compensate for massive loss of 
absorbing surface. 

In 1965, Keller (13) began experimenting with paired reversed 
segments in dogs with a 90% enterectomy, and concluded that it was a 
superior procedure metabolically. In 1967, Fink and Olson (14) reported 
favorably on a patient to whom they had given two reversed segments to 
compensate for the "short bowel syndrome". 

Much attention has been given to the optimum site for insertion 
of the reversed segment. Although Singleton (15) suggested in 1961 that 
a proximal enterectomy resulted in less steatorrhea and malnutrition 
than a distal enterectomy in dogs, subsequent metabolic and absorptive 
studies have shown the proximal small intestine to be the site of maxi¬ 
mal aibsorption. In 1948, Cogsv^ell (16) had demonstrated in dogs that 
inanition occurred more often after proximal than distal small in¬ 
testinal resection. Borgstrom's (17) experiments in 1957 showed that 
the process of absorption of fat, carbohydrate and protein starts in the 
duodenum, and is complete after 100 era. of jejunum. The conclusion 


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113 

reached by Baldwin Price in 1965 (18) was that the proximal small 
intestine has a greater absorptive capacity than the distal, and that 
this capacity decreases from above downwards. 

Unfortunately, the maximum length of reversed segment possible 
without causing obstruction increases from above downwards, as shovm 
by Stahlgren in 1962 (9). He demonstrated in dogs that jejunal seg¬ 
ments of no more than two inches could safely be reversed, while ileal 
segments of three to four inches were permissible. (This restriction 
refers only to reversal of small intestine, and not stomach. Poth (19) 
has shown that large antiperistaltic pouches of jejunum, fashioned in 
nimerous different v/ays, may be used as gastric substitution pouches, 
and are compatible with ordinary alimentation and excellent nutrition). 

Thus, the favored site for insertion of an antiperistaltic 
segment, if there were a choice, would be at a point about 90 cm. 
distal to the Ligament of Treitz, a conclusion arrived at independently 
by Madding (1965) (20), and Shepherd (1966) (21). "It would seem 

physiologically sound to delay the passage of food through this segment 
in which the concentration of enzymes is highest and absorption 
greatest" said Madding (20), referring to the first 90 cm. of jejunum. 

The time available for absorption of intra-luminal contents 
will be proportional to the length of the intestine through which it 
passes. Although this time will be the same for all the intestinal 
contents, certain metabolic deficiencies are more keenly felt in the 
early stages post enterectomy. Thus, fat absorption has been shown to 
be more impaired than protein or carbohydrate absorption in patients with 


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114 

"short bowel syndrome". Other early metabolic sequelae are deficiencies 

of Vitamins C, and calciijm, elements thought to be absorbed by 

the proximal small intestine. In addition to segmental reversal, 

supplementary supplies of these substances have been advocated 

(Althausen, 1949 (22); Singleton, 1961 (15)), and in the case of lack 

of fat absorption, oral medium-chain triglycerides have been shown to 

/ 

enhance weight gain and reduce the incidence of steatorrhea. 

(Winawer, 1966) (23). 

Encouraging results from experimental work has resulted in 
clinical trials of reversed intestinal segments. Sixteen cases have 
been reported in the literature.(24, 25, 26, 27). Six of these have 
been after resection for Crohn's disease, the most recent of these 
requiring the reversed segment to be removed, for a recurrence of the 
disease process, and another segment reversed. (Fink and Olson, 1967). 
Four have followed mesenteric infection, two have resulted from 
numerous resections for adhesions, and one, three resections in the 
gastrointestinal tract for recurrent carcinoma. Severe diarrhea has 
stimulated three reversals, the most recent of these being the post 
ileostomy diarrhea of a woman whose colon and distal ileiim had been 
resected for ulcerative colitis. Her ileostomy output equalled 90% of 
her intake. Dramatic improvement followed reversal of a 10 cm. segment 
just proximal to the ileostomy, but after six months gradual relaxation 
of the segment has produced a return to the preoperative level, and the 


long term result appears poor. 






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115 


FOOTNOTES 


MALL, F.P. Reversal of the intestine. Johns Hopkins Hosp. 
Rep . , _1: 93 , 1896 . 

2 

HALSTED, W.S. Circular suture of the intestine - an 
experimental study. Am. J. Med. Sc., 9^:436, 1887. 

3 

IVY, A.C. A brief review of the physiology of the duodenum. 
Radiology, 9_:47-59, 1927. 

4 

HAI'IMER, J.M., and HILL, E.J. Experimental ulcer produced by 
reversing the duodenum. Harper Hosp. Bull., 9:129-131, 1951. 

5 

HAMMER, J.M., VISSCHER, J., and HILL, E.J. Experimental 
gastrojejunal ulcers produced by reversing the duodenum. Arch. Surg., 
£^:23~28, 1953. 

6 

HAMMER, J.M., SEAY, P.H., HILL, E.J., PRUST, F.W., and 
CAMPBELL, R.B. Intestinal segments as internal pedicle grafts. 

Arch. Surg., 7^:625-642, 1955. 

7 

HAJ4MER, J.M., SEAY, P.H., JOHNSTON, R.L., HILL, E.J., PRUST, 
F.H., and CAMPBELL, R.J. The effect of antiperistaltic bowel segments 
on intestinal emptying time. AMA Arch. Surg., 7^:537-541, 1959. 

g 

SINGLETON, A., and ROWE, E. Peristalsis in reversed loops 
of boivel. Ann. Surg., 139:853, 1954. 


9 

STAHLGREN, L.H,, UMANA, G., ROY, R., and DONNELLY, J. A 
study of intestinal absorption in dogs following massive small 
intestinal resection and insertion of an antiperistaltic segment. 
Ann. Surg., 156:483-492, 1962. 


^^SAKO, K., GERSZI, K., and MARCHETTA, F.C. Nutritional effects 
of a short reversed jejunal segment. Arch. Surg., 89:1102-1105, 1964. 




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116 


11 

MACKBY, M.J., RICHARDS, V., GILFILLAN, R.S., and FLORIDIA, R. 
Methods of increasing efficiency of residual small bowel segments: a 
preliminary study. Am. J. Surg., 109:32-38, 1965. 


12 


Ibid. 


13 

KELLER, J.W., STEWART, W.R.C., WESTERIIEIDE, R,., and 
PACE, W.G. Prolonged survival with paired reversed segments after 
massive intestinal resection. Arch. Surg., 174-179, 1965. 

14 

FINK, W.J., and OLSON, J.D. The massive bowel resection 
syndrome: treatment with reversed intestinal segments. Arch. Surg., 

94:700-706, 1967. 


SINGLETON, A., and KURRUS, F. The increasing of absorption 
following massive resections of bowel by means of antiperistaltic bowel 
segments as measured by radioiodine fat absorption studies. Ann. Surg., 
154:130, 1961. 


COGSWELL, H. Massive resection of the small intestine. 
Ann. Surg., 127:377, 1948. 


BORGSTROM, B. Studies of intestinal digestion and absorption 
in the human. J. Clin. Invest., 36:1521, 1957. 

18 

BALDWIN-PRICE, H.K., COPP, D., and SINGLETON, A.O., Jr. 

Reversed intestinal segments in the management of anenteric malabsorption 
syndrome. Ann. Surg., 161:225-230, 1965. 


19 

POTH, E.J., and SMITH, L.B. Digestion and absorption follow¬ 
ing gastrectomy using reversed jejunal segments: follow up of 50 cases. 
Ann. Surg., 163:957-960, 1966. 


20 

MADDING, G.F., KENNEDY, P.A., and McLAUGHLIN, R.T. Clinical 
use of antiperistaltic bowel segments. Ann. Surg., 161 :601-604, 1965. 


21 

SHEPARD, D. Antiperistaltic bowel segment in the treatment 
of the short bowel syndrome. Ann. Surg., 163 :850-855, June, 1966. 


22 

ALTHAUSEN, T.L., UYEYAMA, K., and SIMPSON, R.A. Digestion 
and absorption after massive resection of small intestine. 
Gastroenterology, 12:795, 1949. 









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117 


23 

WINAI^R, S.J., BROITMAN, S.A., WOLOCHOW, D.A., et al. 
Successful management of massive small bowel resection based on 
assessment of absorptive defects and nutritional needs. New Eng. 

Med. J., 274 :72-78, 1966. 

24 

VENABLES, C.W,, ELLIS, H., and SMITH, A.D.M. Antiperistaltic 
segments after massive intestinal resection. Lancet, 2:1390-1394, 1966. 

25 

BRAASH, J.W., and SEDGWICK, C.E. Reversed loops in the short 
bowel syndrome. Lahey Clin. Found. Bull., ]^: 27-3 2, 1965. 

2 6 

FINK, W.J., and OLSON, J.D, The massive bowel resection 
syndrome: treatment with reversed intestinal segments. Arch. Surg., 

9^:700-704, May 1967. 

27 

WILMORE, D.,W., and JOHNSON, C.J. Metabolic effects of 
small bowel reversed in treatment of the short bowel' syndrome. 

Arch. Surg., 97:784-791, November, 1968. 




‘/I 








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METHODOLOGY 


I. General 

Adult mongrel dogs of both sexes, weighing 13 - 25 kg. were 
used. Before being released to the laboratory, the animals had been 
kept at the Health Sciences Animal Center for two weeks for assessment 
of general condition. After receiving vaccination against canine 
hepatitis and distemper, deworming, and being passed as fit, they were 

brought to the Surgical-Medical Research Institute for the experiment. 

• ^ 

Their daily diet consisted of one can of commerical dog food daily, 

and unlimited water. Daily outdoor exercise was provided. Any dogs 
which became ill during the course of the experiment were excluded 
from the study. 

II. Experimental Plan 

All six dogs were provided with a Heidenhain Pouch. Control 
body weights and Heidenhain Pouch secretions were recorded daily on 
these dogs for a month under various conditions and gastric emptying 
time was measured radiologically. After this a ninety per cent 
enterectomy was performed on all of them. Body weights, Heidenhain 
Pouch secretions, and gastric emptying times were again measured under 
identical conditions. Finally, an eight centimeter segment of jejunum 
was reversed, and reinserted into alimentary continuity in an. anti- 

* 

Dr. Ballard’s 


118 









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119 

peristaltic direction, and further measurements made of body v/eight, 
Heidenhain Pouch secretion and gastric emptying times, under the 
same sets of conditions. 

Ill . Before Operation 

Good general health was the criterion for surgery. Careful 
preoperative examination was carried out to ensure this, and the dog 
allowed to exercise up until the day of the surgery. Food was withheld 
for twenty-four hours before the procedure, and water for twelve hours. 


IV. Operation 

In the preparation room, a superficial vein was displayed by 
shaving part of the leg, and anaesthesia induced by the intravenous 
administration of Nembutal, 30 mg,/kg. body weight. A cuffed endo¬ 
tracheal tube was then inserted with a laryngoscope, under direct vision. 
The hair was removed from the abdominal skin with an electric razor, 
and the skin scrubbed with soap and warm water. The dog was then carried 
into the operating room, placed supine on the operating table with a 
leg tethered to each corner, and the operative site prepared with 
Betadine solution. Drapes were applied in the usual manner, strict 
sterile technique being maintained at all times. Care was taxen to 
enter the abdomen through the linea alba, to facilitate a relatively 
bloodless entry, the incision being made from xiphisternum to umbilicus 
for Heidenhain Pouch construction, and more caudally for operations on 


the small intestine. 




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120 


V. Heidenhain Pouch Construction (Figure 1) 

A search of the abdominal cavity was first made to exclude 
any unsuspected pathology. When none was found, the serosa of the 
stomach was exposed by gentle displacement of the omentum, and non¬ 
crushing clamps applied to contain a generous wedge from the fundic 
area of the greater curvature, the point of the wedge being equi¬ 
distant from both curvatures. Defects were created in the omentum to 
enable the wedge to retain a blood supply when separated from the main 
stomach, and occasionally the ligation and division of a marginal 
artery was necessary to make these openings large enough. 

The mucosa pouting through the teeth of the clamps on the 
main stomach was then sewn together with 3-0 catgut, the clamps removed, 
and the serosal edges co-apted with a running suture also of 3-0 
chromic catgut to bury the m.ucosal suture line. A similar procedure was 
performed on the resected wedge, except that before the pouch was 
completely closed, a stainless steel cannula was placed inside it, and 
the end brought out through a separate incision. The cannulated pouch 
was then allov/ed to rest without tension against the internal abdominal 
wall, and the end of the cannula brought out through the abdominal wall 
in a suitable place to drain freely. Interrupted sutures were used to 
fix the pouch in this position, and after a final check for hemostasis, 
the abdomen was closed in layers. 

VI. Enterectomy (F igure 2) 

The small intestine was delivered from the abdomen from the 
Ligament of Treitz to the junction with the cecum, and its length 






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HEIOENHAIN POUCH 


Fig. 1.—^Heidenhain Pouch 





90% OF SMALL 
NTESTINE EXCISED 



ENTERECTOMY 


Fig. 2.—Massive Enterectomy 












123 


measured with a ruler. The average length was 300 cm. Five per cent 
of this length was measured distally from the Ligaiaent of-Treitz, and 
five per cent proximally from the ileocecal junction, and non-crushing 
clamps applied at these two places. The mesenteric vessels lying between 
these two points were ligated in continuity and divided, and the intes¬ 
tine between these two points resected, to include the wall that was held 
in the teeth of the clamps. A two layer end-to-end anastomosis was 
then performed, using 4-0 chromic catgut for the mucosa, and 3-0 silk 
for the serosal layer. The mesenteric defect was repaired with inter¬ 
rupted sutures of 3-0 chromic catgut to prevent possible herniation. 

The anastomotic lumen was checked for patency, and the anastomosed 
bowel for viability. Hemostasis was secured, and the abdomen closed in 
layers, using an absorbable subcuticular suture for the skin to obviate 
the need for subsequent suture removal with its disturbing effect on the 
experimental subject. 

VII. Segmental Reversal (Figure 3) 

The shortened small intestine was withdrawn from the abdominal 
cavity after freeing any adhesions tethering it. An eight centimeter 
length v;as selected immediately distal to the Ligament of Treitz, the 
vascular supply of v/hich would lend itself to torsion without compromising 
it. On either side of these vessels, defects were created in the 
mesentery parallel with the vessels, and the integrity of the blood 
supply confirmed by prolonged inspection. Paired non-crushing clamps 
v/ere then applied to the intestine immediately distal to these defects, 






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125 


where the surface had been gently cleared of fat. The bowel was then 
cut across at these two places as a continuation of the tv/o mesenteric 
rents, turned on its vascular pedicle through 180 degrees, and ali¬ 
mentary continuity restored by end-to-end anastomosis. Chromic catgut 
4-0 was used to approximate the mucosa, and 3-0 silk for serosal layer, 
all these sutures being interrupted. The patency of the lumen was 
established by palpation, and the viability of the segment by in¬ 
spection before the abdomen was closed in layers, using a subcuticular 
chromic catgut suture for skin closure. 

VIII. Postoperative Management 

Immediately at the conclusion of every surgical procedure, the 
dogs were covered with a spare drape, and the operating room lights 
used to supply warmth while they regained consciousness. This was in¬ 
strumental in diminishing the violent shivering known to accompany re¬ 
covery from Nembutal anaesthesia in dogs. Wtien the orbital reflex had 
returned, and the level of anaesthesia had become sufficiently light 
for the swallowing reflex to be demonstrable, the dog was extubated. 

On recovery of consciousness, the animals were returned to their runs. 

Fluids were given intravenously for the first three days after 
surgery, as 30 ml./kg. of 5% dextrose saline. During the third day, 
water was offered in a bowl, which the dogs invariably took well by 
mouth. Milk, pablum, and Heinz clear consomme were given as tolerated, 
and the dogs had resumed normal feeding by the sixth postoperative day. 
One gram of calcium carbonate was included in the diet to lessen the 


inevitable diarrhea. 



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126 


To minimize the distortion of results by infection, prophylactic 
antibiotics were used. Ten millograms per kilogram of "Fortimycin", 
a mixture of penicillin and streptomycin, were given before surgery, 
and daily thereafter for three days. Normal exercise was resumed at 
this time. 

No testing was undertaken until three weeks after every surgical 
procedure, and the dog was carefully assessed during this recovery time. 
Pouch secretions were then collected when the dog had completely re¬ 
covered from the insult. 

Gastric emptying times were measured radiologically, during the 
control period, following enterectomy, and after insertion of the anti- 
peristaltic segment. Abdominal x-rays were taken immediately after the 
dog had eaten a meal consisting of 50 gm. of commercial dog meat mixed 
with 50 ml. of liquid barium. Hourly x-rays were taken thereafter, 
and the end point taken as the time when only traces of the mixture 
remained in the stomach. 

IX. Collection of Samples 

Bard rubber bladders were fitted with an attaclmi^ent enabling 
them to be fixed to the metal cannula draining the secretions of the 
Heidenhain Pouch to the exterior. To obtain the twenty-four hour 
samples, the bladder was fitted to the cannula at 5:00 p.m. one evening, 
and removed at 5:00 p.m. the following evening. The bladders were 
protected by muzzling the dogs, which were only removed for feeding, 
while the animals were under observation. The twenty-four collections 




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127 


took place under .normal conditions of activity in the animal house. For 
the fed collections, the dogs were given eight ounces of Dr. Ballard's 
dog food twice during the day. 

For the eight hour awake collections, the bags were fixed on 
at 9:00 a.m., emptied at hourly intervals until 5:00 p.m., and protected 
by muzzling the dogs. 

For the eight hour anaesthetized collections, the dogs were 
given Nembutal intravenously, 30 mg./kg. and an endotracheal tube in¬ 
serted. They were laid on their left side, with the cannula draining 
into the rubber bladder, and the contents emptied and measured hourly. 
Hydration was maintained by intravenous infusion of 5% dextrose saline 
at 5 ml./kg./hr. For the fed anaesthetized collections, a homogenate 
of 120 gm. of Dr. Ballard's dog food and 80 ml. distilled water was 
infused into the stomach via orogastric tube at the end of the second 
hour. 

At every collection, the bladders were carefully inspected, for 
leakage or damage, and that sample discarded if any were found. 

X. Laboratory Procedures 

Determcination of gastric acidity .-- The volume of every sample 
was measured and recorded. The quantity of free and total acid in the 
secretions was determined by the following method; one milliliter of 
the sample was pipetted into a titration vessel in an autoburette, and 
the pH measured automatically by a pH meter. 




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The radiometer automatic titrator was then connected to the 
autoburette, and N/10 sodium hydroxide automatically added to the 
sample until a pH of 4.0 was reached, at which time the amount of free 
acid was indicated on a dial on the autoburette. 

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continued the titration to pH 7.0, when the amount of total acid 
present in the sample appeared on the same scale on the autoburette. 

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hydroxide added to bring the pH to 4.0 and 7.0 respectively was directly 
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1. 


RESULTS 


l. Twenty-Four Hour Heidenhain Pouch Secretions 

Control The mean total twenty-four hour postprandial Heiden¬ 
hain Pouch secretion of 74 ml. in this category is in keeping with the 
range found by other investigators. The mean free acid concentration was 
6.5 m.Eq./vol. and the mean total acid concentration was 7.5 m.Eq./vol. 

The mean twenty-four hour total fasting Heidenhain Pouch secretion 
of 65 ml. is within the expected range, and is predictably less than the 
postprandial mean volume. There was a corresponding decrease in the mean 
free acid concentration, which was 6.1 m.Eq./vol. and the mean total acid 
concentration, which was 6.5 m.Eq./vol. 

After massive ent erec t omy .— The mean total twenty-four hour 
total postprandial Heidenhain Pouch secretion rose to 162 ml., the mean 
free acid concentration to 21 m.Eq./vol. and the mean total acid con¬ 
centration to 24 m.Eq./vol. (Figure 4). All three increments were 

s * 

statistically significant (p = 0,01) (Table 1, 1 ) 

The mean total tv/enty-four hour fasting Heidenhain Pouch 
secretion rose to 90 ml, the mean free acid concentration to 9.5 

m. Eq./vol. and the mean total acid concentration to 10.4 m.Eq./vol. 

(Figure 4). None of these increments was statistically significant 
(Table 2, 2^) 

* s s 

Statistical analysis (Tables 1 -6 ) appears at the end of this section. 


129 






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131 


TABLE l.--Mean Total Twenty-Four Hour Awake Postprandial Heidenhain 
Pouch Secretory Volumes, Free and Total Acid Concen¬ 
trations, in Control Dogs, Enterectomized Dogs 
(Group A), and Dogs with an Antiperistaltic 
Jejunal Segment (Group B). Statistically 
Significant Increases (p = 0.01) were 
Noted in Heidenhain Pouch Secretory 
Volume, Free and Total Acid Con¬ 
centrations, After Both 
Operative Procedures 



Control 

Group A 

P value"^ 

Group B 

-t 

P value 

* 

Volume , 

T 

Free Acid 

74.5 

162,2 

0.01 

283.2 

0.01 

6.48 

20.64 

0.01 

39.37 

0.01 

Total Acid* 

1 

7.54 

23.77 

f—1 

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0.01 


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Volume in ml. 


j 

Acid in m.Eq./vol. 

4 ^ 

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132 


TABLE 2.—Mean Total Twenty-Four Hour Awake Fasting Heidenhain Pouch 
Secretory Volumes, Free and Total Acid Concentrations, 
in Control Dogs, Enterectomized Dogs (Group A), and 
Dogs with an Antiperistaltic Jejunal Segment, 

No Statistically Significant Change 
Following Enterectomy, but After 
Insertion of the Reversed 
Segment, Significant 
Changes were Noted 
in Heidenhain Pouch 
Secretory Volume, 

Free and Total 
Acid Con¬ 
centrations 
(p-0,05) 



Control 

Group A 

P value 

Group B 

- 

•t 

P value 

* 

Volume , 

; t 

! Free Acid 

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90,5 

N.S . 

203.2 

0.05 

6,10 

9.50 

N,S. 

23.72 

0.05 

Total Acid' 

6,50 

10.37 

N.S . 

27.36 

0.05 


* 


Volume in ml. 

i 

Acid in m,Eq./vol. 
f- 

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133 


After segmental reversal .-- The mean total twenty-four hour 
postprandial Heidenhain Pouch secretion underwent a further rise, to 
283 ml. The mean free acid concentration rose to 39 m.Eq./vol. and 
the mean total acid concentration rose to 41 m.Eq./vol. (Figure 4) . 

All three increments were statistically significant as compared with the 
control secretions (p = 0.01) (Table 1). Compared with the post- 
enterectomy secretions, the increases in the volume and free acid 
secretions were significant (p = 0.05), but the increase in total 
acid concentration was not significant. (Table 1®) 

The mean total twenty-four hour fasting Heidenhain Pouch 
secretions rose further to 203 ml. following insertion of an anti- 
peristaltic segment. The mean free acid concentration rose to 24 
m.Eq./vol. and the mean total acid concentration rose to 27.4 m.Eq./vol. 
(Figure 4). Compared with the control figures, all three increments 
were statistically significant (p = 0.05) (Table 2). Compared with the 
postenterectomy figures, only the rise in mean total acid concentration 

o 

was statistically significant (p = 0.05) (Table 2 ), 

II. Eight Hour Awake Heidenhain Pouch Secretions 

Control.-- The mean total eight hourly postprandial Heidenhain 
Pouch secretion was 36.4 ml. The mean free acid concentration was 4.2 
m.Eq./vol. and the mean total acid concentration was 4.5 m.Eq./vol. 

The mean total eight hour fasting Heidenhain Pouch secretion 
was 9.5 ml. The mean free acid concentration was 0.27 m.Eq./vol. and 
the mean total acid concentration was 0.29 m.Eq./vol. 





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134 


After massive enterectomy .— The mean eight hour total post¬ 
prandial Heidenhain Pouch secretion decreased slightly to 35.8 ml. The 
mean free acid concentration however rose to 4.7 m.Eq./vol. and the mean 
total acid concentration rose to 4.9 m.Eq./vol. (Figure 5). None of 
these changes was statistically significant (Table 3, 3®). 

The mean eight hour total fasting Heidenhain Pouch secretion 
also decreased to 8.6 ml. Despite this fall in secretory volume, the 
mean free acid concentration, however, rose to 0,44 m.Eq./vol. and the 
mean total acid concentration rose to 0.51 m.Eq./vol. (Figure 5). 

None of these changes was statistically significant. (Table 4, 4 ). 

After segmental reversal .— The mean total eight hour post¬ 
prandial Heidenhain Pouch secretion underwent another small decrease 
after insertion of an antiperistaltic segment of small intestine, 
falling to 34.34 ml. The mean free acid concentration now fell to 
below the control level, reaching 3.96 m.Eq./vol. while the mean total 
acid concentration fell to 4.21 m.Eq./vol.—also less than the control 
figure (Figure 5). None of these changes was statistically significant 
(Tables 3, 3^) . 

The mean total eight hour fasting Heidenhain Pouch secretion 
remained unchanged at 8.65 ml. after segmental reversal (Figure 5). 

The mean free and total acid concentrations were also unaffected by 
this procedure, remaining at 0.44 m.Eq./vol. and 0.51 m.Eq./vol. 

(Table 4, 4^) . 





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136 


TABLE 3,—Mean Total Eight Hour Awake Postprandial Heidenhain Pouch 
Secretory Volumes, Free and Total Acid Concentrations, 
in Control Dogs, Enterectomized Dogs (Group A) and 
Dogs with an Antiperistaltic Jejunal Segment 
(Group B)- None of the Heidenhain Pouch 
Secretory Changes Following Either 
Procedure was Statistically 
Significant 



Control 

Group A 

P value 

Group B 

•t- 

P value 

* 

Volume . 

T 

Free Acid 

Total Acid 

36.4 

35.8 

N.S . 

34.3 

N.S . 

4,24 

4.69 

N.S . 

3.96 

N.S . 

4.45 

4.88 

N.S, 

4.21 

N.S . 


* 


Volume in ml. 

Acid in m.Eq./vol. 

Statistical significance of the change as compared with control figures. 




















i 




f 




'/ ■ w.' 


f ( 


t- 


'•if 



i 


r ^ 

• %f 


* ;• 

•gf i-^r-Ai 

i,' t / ^ ' ,• 





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rt’>/K t ! f> C » I 

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.,. ~ • ^ -41 

^ • ’"'Mi 

Ij ‘rfK—,e S 40 >\T 

' • f'.'V' Y 

J foXTtfoO Cfi _ 


4 • 


















137 


TABLE 4.-'-Mean Total Eight Hour Awake Fasting Heidenhain Pouch Secretory 
Volumes, Free and Total Acid Concentrations, in Control Dogs, 
Enterectomized Dogs (Group A), and Dogs with an Antiperi- 
staltic Jejunal Segment (Group B), No Statistically 
Significant Secretory Change was Observed After 

Either Procedure 



Control 

Group A 

-t 

P value 

Group B 

P value 

* 

Volume 

9.5 

8.7 

N.S . 

8.7 

N.S . 

Free Acid', 
t 

Total Acid 

0,27 

0.43 

N.S . 

0.44 

N.S . 

0.29 

0.50 

N.S . 

0.51 

N.S . 


ic 

Volume in ml. 


1 

Acid in m.Eq./vol. 

Statistical significance of the change as compared with control figures. 

















Vll 



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.'TO J 


Js 






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r 





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11.9 



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138 


III. Eight Hour Anaesth et ized Heidenhain Pouch Secretions 

Control.-- The mean total eight hour postprandial Heidenhain 
Pouch secretion was 34,1 ml. The mean free acid concentration was 3.94 
m.Eq./vol,, and the mean total acid concentration was 4.13 m.Eq./vol. 

The mean total eight hour fasting Heidenhain Pouch secretion 
was 16.7 ml. The mean free acid concentration was 0.67 m.Eq./vol. 
and the mean total acid concentration 0,80 m.Eq./vol. 

After massive enterectomy .— After enterectomy, the mean total 
eight hour postprandial Heidenhain Pouch secretion rose to 52.6 ml. The 
mean free acid concentration rose to 6.70 m.Eq./vol. and the mean total 
acid concentration to 6.96 m..Eq./vol. (Figure 6). None of these changes 

g 

v/as statistically significant (Tables 5, 5 ) , 

The mean total eight hour fasting Heidenhain Pouch secretion 
rose to 28.5 ml. after enterectomy. The mean free acid concentration 
rose markedly to 2.73 m.Eq./vol, and so did the mean total acid con¬ 
centration, to 2.88 m.Eq./vol, (Figure 6). None of these changes was 

g 

statistically significant (Tables 6, 6 ) . 

After segmental reversal .— Following insertion of the anti- 
peristaltic segment, the mean total eight hour postprandial Heidenhain 
Pouch secretion rose to 73.9 ml. The mean free acid concentration rose 
to 9.94 m.Eq./vol., and the mean total acid concentration rose to 
10.02 m.Eq./vol. (Figure 6), 

The mean total eight hour fasting Heidenhain Pouch secretion 
after insertion of an antiperistaltic segment remained unchanged at 28.55 
ml. Similarly, the free and total acid concentrations were unaffected 

g 

by the procedure. (Tables 6, 6 ). 







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l\biiu &*mf Li i mcf^ f.m 

HRaXktJST) ,c*tj4«»ooxq art:) 




■• xk 













CONTROL POST ENTERECTOMY POST REVERSAL 

MEAN HEIDENHAIN POUCH SECRETIONS OF FED & FASTING DOGS ANAESTHETISED DURING 8 HRS. 


Fig. 6.—Effect of enterectomy and subsequent insertion of an 
antiperistaltic segment on mean total eight hour Heidenhain Pouch 
secretory volumes in anaesthetized dogs. No statistically significant 
changes were observed after either procedure. 























I * • •Wl 





r M, 


.'4 


i, 







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4«) 






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iaiattvA4v.4. ,A-. . 














140 


TABLE 5.—-Mean Total Eight Hour Anaesthetized Postprandial Heidenhain 

Pouch Secretory Volumes, Free and Total Acid Concentrations, 
in Control Dogs, Enterectomized Dogs (Group A), and Dogs 
with an Antiperistaltic Jejunal Segment (Group B). 

None of the Secretory Changes Following Either 
Procedure was Statistically Significant 



Control 

Group A 

P value 

Group B 

+ 1 

P value i 

* 

Volume 

34.1 ' 

52.6 

N.S . 

74.0 

N.S. 

Free Acid' 

3.94 

6.70 

N.S . 

9.94 

N.S . 

Total Acid' 

4.13 

7.00 

N.S . 

10.03 

N.S . 


* 


Volume in ml, 

Acid in m.Eq./vol. 

Statistical significance of the change as compared with control figures. 

























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141 


TABLE 6.—Mean Total Eight Hour Anaesthetized Fasting Heidenhain Pouch 
Secretory Volumes, Free and Total Acid Concentrations, 
in Control Dogs, Enterectomized Dogs (Group A), and 
Dogs with an Antiperistaltic Jejunal Segment 
(Group B). None of the Secretory Changes 
Following Either Procedure was Found 
To Be Statistically Significant 



Control 

Group A 

4* 

P value 

Group B 

P value 

* 

Volume 

t 

Free Acid 

Total Acid”^ 

16.7 

28.5 

N.S . 

28.5 

N.S . 

0.67 

2.72 

N.S . 

2.72 

N.S . 

0.80 

2,88 

N.S . 

2.88 

N.S . 


* 


Volume in ml, 

1 * 

Acid in m.Eq./vol. 

Statistical significance of the change as compared with control figures, 





















rv 


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••I. 






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va 


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142 


^^• Body Weights 

At the beginning of the experiment, in January, 1969, the 
mean body weight of the dogs equipped with their Heidenhain Pouch, 

was 19.2 kilos. Immediately after massive enterectomy, the body weights 

of the dogs began to decline steadily, in the way described by previous 
investigators. (1) By the 49th postenterectomy day, in March 1969, the 
mean weight had fallen to 15.8 kilos (82% of the original figure) , and 
was continuing to fall. 

It was at this stage that the antiperistaltic segment was in¬ 
serted, with the downward trend well established, but while the dogs 
were still able to withstand surgery. The weight loss continued, but at 

a reduced rate. By the 49th postreversal day, in May, 1969, the mean 

weight of the dogs had levelled off at 14,4 kilos (75% of the original 
figure). Two weeks later, at the conclusion of the experiment, this 
mean weight had not changed, (Figure 7) . 

V. Gastr ic Emptying Times 

Controls.— The mean transit time for a mixture of 50 gm. meat 
and 50 ml. of barium to empty from the stomach in the control group of 
dogs was three hours. The stomach-was considered empty when only traces 
of the meal remained visible in the lumen. Figure 8 shov/s the plate 
taken shortly after dog 1359 had swallowed the mixture, on the left; 
and on the right, the three hour plate, when the emptying process is 


complete. 







» • ^ 





I 


I) ■ X. 

'H'; ' 




ir. 




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1» •y-'-aii J ‘ 1 **•;? > •-, 14,'fl lo .Jn» 02 Ewns^ 

ftwOftyJ vln'v •••■ '•“'■ A^‘' .’• '• ii’>jw?'^e frifl' ■ »*n/l4^ b«w ^ 90 i>’^ 

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REVERSED 

SEGMENT 


* 




CONTROL POST- POST- POST- 

(JANUARY) ENTERECTOMY REVERSAL REVERSAL 

(MARCH) (MAY) (JUNE) 

EFFECT OF ENTERECTOMY & REVERSED JEJUNAL SEGMENT ON MEAN BODY WEIGHT 

OF 6 DOGS 


Fig. 7,—Comparison of the mean body weights of dogs before 
enterectcwiy, two months after massive enterectomy, and two and three 
months after reversal of a jejunal segment. 

















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145 


Aj-ter_maj^ ye enterectom y.—• Following enterectomy, the mean 
gastric emptying time was unchanged from the control figure of three 
hours. On the left. Figure 9 again shows the stomach of the enterec- 
tomized dog 1359 a few minutes after swallowing the same quantity of the 
barium mixture; and the same stomach three hours later, on the right, 
when only traces of the meal are visible within the stomach. 

After segmental reversal .-- Following insertion of an anti- 
peristaltic jejunal segment, transit time was delayed. Figure 10 show^s 
on the left, the stomach of dog 1359 soon after swallowing the same 
amount of the barium mixture. The x-ray on the right, taken three hours 
later, shows a large proportion of the meal remaining in the stomach. 
Serial x-rays were taken hourly, and it was not until the six hour 
plate that the emptying of the stomach was seen to be near completion 
(Figure 11). Tne postreversal emptying times were spread over five to 
seven hours, six being the mean. Dog 1359 was typical. 

The profuse diarrhea that followed massive enterectomy, and 
persisted in spite of oral calcium carbonate therapy (1 gm. daily in 
the food), was markedly reduced following the insertion of an anti- 
peristaltic segment, and in some cases, the dogs produced semi—formed 


stools. 















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Fig. 10.—Barium x~rays of dog 1359 after insertion of an anti- 
peristaltic segment. The plate on the left shows the stcmach a few 
minutes after the dog had swallowed the barium mixture. The plate 
on the right shows the same stomach remaining partially full three 
hours later. 










Fig. 11.—Barium x-ray of dog 1359 after insertion of an anti- 
peristaltic segment. The stomach is almost empty of the barium 
mixture at six hours after its ingestion, demonstrating a long delay 
in gastric emptying after segmental reversal. Also see Figure 10. 





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149 


FOOTNOTES 


^REUL, G.J., 
resection on gastric 


and ELLISON, E.H. 
secretion. Am. J. 


Effect of 75% distal small bowel 
Surg., 111:772, 1966. 




- 14 *^ 



TABLE 1 .—Statistical Analysis of the Changes in Twenty-four Hour Total Awake Postprandial Heidenhain Pouch Secretory Volumes, Free and Total Acid 

Concentrations, in Control Dogs (El), Enterectomized Dogs (E2) and Dogs with an Antiperistaltic Jejunal Segment (E3) 


1 

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TABLE 2 .—Statistical Analysis of the Changes in Twenty-four Hour Total AwaXe Fasting Heidenhain Pouch Secretory Volumes, Free and Total Acid 

Concentrations in Control Dogs (El), Enterectomized Dogs (E2), and Dogs with an Antiperistaltic Jejunal Segment (E3) 




0) 




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TABLE 3 .—Statistical Analysis of the Changes in Eight Hour, Hoxirly AwaJce Postprandial Heidenhain Pouch Secretory Volumes, Free and Total Acid 
Concentrations, in Control Dogs (El), Enterectanized Dogs {E2) and Dogs with an Antiperistaltic Jejunal Segment CE3) 


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2 2 2 <H 2 2 2 2 


COCOCOtJ^COCOCOCO 

222 Ln 2222 


•^r^-rHcrvcrkr^r^rH 

r^'xmcoor'^cN 

^cocD^foinvorH 

OiHOCNrHOOO 


mr^r^oocj^inr' 

rH 4-4 OCNrHOOO 


cf>cx)in»^r^coHro 

rOM'cTrHCOcOr-CO 

co^fHCNininvDCN 

0*-40f'4»H000 


U 

w 

• • 



























a 


fH 



























0 


U 



0 

CO 

ro 

in 

in 

CD 

CO 

0 

04 

CD 


H 

CO 

fH 

ON 

04 

CD 

O' 

O' 

in 


fH 



X 



<U 

u 


CT' 

CO 

m 


rH 

0 

ro 

rH 


O) 

n 



O' 

(V) 

04 


0 



m 


O' 


p 

«H 

w 


fH 

cD 


fH 

0 

fH 


m 

in 

fH 

0 

m 

0 

04 

m 

CO 

CD 

rH 

rH 

CD 

0 

04 

CD 

CO 

O' 

JZ 

cn 

H 



c 

0 

'O 

n 3 

> 

u 

fH 

0 

ro 

fH 

04 

ro 

in 


0 

0 

0 

0 

0 

0 

0 

0 

0 

0 

0 

0 

0 

0 

0 

0 

CA 


























cu 

5 r 


•H 

Q) 


























0 

Q 


p 

P 

in 

ro 

ro 


O' 

CO 

0 

CD 

03 

CO 

ro 

lO 

0 

CO 

ON 

04 

03 

O' 

04 


m 



0 

c 


c 

c: 

O' 

04 

0 

CT' 

0 

C '4 

CD 

CD 

in 

iH 

0- 

04 

CD 

04 

ro 

fH 

ro 



ro 

O' 


ON 


-H 



0 

•H 

CN 

«H 

0 

0 

fH 

in 


0 


m 

O' 

0 

in 

0 


00 

ro 

in 

O' 

CO 

O' 


CD 

0 


*H 


u 
























CA 

0 




ro 


CO 

CN 

0 

CD 

a> 

in 

0 

0 

0 

04 




0 

0 

0 

0 





rH 

0 ) 

H 







iH 

fH 





















I I I I I I I I 


I I I I 



O' 

0 

ro 

O' 

ro 

ro 

O' 

ro 

m 

in 

00 

CO 

in 

ro 

ro 

0* 

P' 

CD 

m 

CN 

O' 

in 

ro 

00 

p' 

CO 

in 

•H* 

CD 

0 

ro 

iH 

ro 

CO 

fH 

ro 

00 

in 

UN 

in 


rH 

0 

O' 

0 

ro 

CO 

CO 

CO 

0 

O' 

04 

04 

ro 

CN 

E3 

O' 

r' 

0 


CO 

CD 

ON 

04 

O' 

ON 

0 


O' 

in 

O' 

04 

rH 

ON 

ON 

O' 


00 

in 

ON 

.H 

fH 

0 

CO 

CD 

0 

ro 

0 

CD 

0 

ON 

ro 

0 

0 

fH 

fH 

rH 

0 

rH 

fH 

ON 

0 

0 




0 


iH 

0 




rH 

fH 

*H 


fH 




















fH 


04 

O' 

in 

in 

m 

0* 

ro 

0 


CD 

0 

O' 


r' 

ro 

O* 

P' 


0 

m 

0 

in 

uo 

CD 

CO 

00 

0 

04 

W 

ON 

rH 

04 

04 

r' 

CO 

ro 

0 

ro 

04 

0 

CD 

ro 

ro 

ro 

V 

m 

0 

O' 

0 


CD 

CO 

CD 

ON 

UN 

CD 

04 

ON 

ro 

rH 


CD 

ro 

U) 

CO 

04 

ro 

cn 

CD 


0 

O' 

un 


rH 

ro 


in 

UN 

0 

0 

cD 

O' 

04 

04 

m 

12 . 

10, 

0* 

r' 


04 

in 

0 

0 

0 

rH 

fH 

fH 

0 

0 

CD 

0 

0 

0 

rH 

fH 

rH 

•H 

0 

CD 


O' 

ON 

0 

vD 

CO 

CO 

04 

04 

04 

CO 


ON 

0 

O' 


04 

CN 

CO 


CO 

CN 


ro 

0 

ON 

O' 

ON 

« 

CO 

CO 

0 

in 

O' 

li) 

04 

04 

iH 

CD 

ro 


0 

ON 

C 3 

O' 

‘D 

ro 

o* 

CO 

vD 

CN 

04 

ro 


ro 

04 

fH 


0 

O' 

in 


04 

rH 

04 

rH 

0 

0 


CD 

P' 

CD 

CD 


ON 

0 

0 


cO 

m 

CO 

CD 

m 


u 




























m m ^ IT) ^ ■• 5 ' 
ro 


OOOOOOOOfO 


OOOOOOOO’^J 





T 3 




'O 


•H 


• 


■H 


0 


•H 


0 


< 


0 


< 




u 

rH 


rH 


rH 

p 

rt 3 

0 

n 3 


n 3 

c: 

P 

Q) 

P 

P 

4 J 

0 

0 

U 

0 

0 

0 

u 

H 

Um 



fci— 

« 


) 


I 


Postenter ectooiy 






























































» ■ 




r 



1 


r 










H 

» s : 

k I 

il 

8 ^ 


I a 
I 8 

;i 

c • 

J? ^ 

Se 

I'i 

rs, 

fs 



1% 
- U 

'E 




T 


~* 



A 


■t 


I 





Ss 





V 


'It 


f- 


'i ='«■■■ 


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TABLE 6 .—Statistical Analysis of the Changes in Eight Hour, I'c- :.naesthatiEod Fasting Heidenhain Pouch Secretory Volumes, Free and Total Acid 

Concentrations, in Control Dogs CEl) , Er.t.- -..-id Doga (E2) and Dogs with an Antiperistaltic Jejunal Segment CE3) 



O 

1 o 

c: 

fO 

to 

CO 

to 

CO 

(0 

10 

to 


CO 

CO 

to 

10 

CO 

CO 

to 

to 


CO 

CO 

to 

to 

to 

CO 

CO 

to 



C <T3 










• 

• 

• 

• 


• 




• 

» 

• 


• 

• 

• 




O' o 

to 'W 


2: 

2 

2 

2 

2 

2 

2 


2 

2 

2 

2 

2 

2 

2 

2 


2 

2 

2 

2 

2 

2 

2 

2 



0) 


vO 

fT) 

CO 



ro 

(N 


O 

O' 



<N 

CN 

CO 

r* 


(N 

in 

O 

CN 

P' 

m 

tn 

rH 



1 p 

<N 

r>- 

rH 


(N 

N* 

N* 

ro 



1/' 

vo 

(N 

VO 

m 


CN 



Tj* 

vo 

CO 

ro 

rH 





H rH 


O' 

<N 


<N 

CN 

vO 

VD 



O' 


CO 

VD 


(O 

vo 


n* 

O' 

o 

CO 

fO 


ro 

VD 
































> 

o 

o 

O 

o 

O 

o 

rH 

O 


o 

o 

O 

o 

O 

o 

o 

o 


o 

o 

o 

o 

O 

o 

rH 

O 


ro 





























W 





























cs 

ta 































C'J 

rH 

VO 


00 


ro 



<o 

CO 

m 

VD 


CN 

m 


vD 

o 

•?? 

iH 

ro 

rH 

VO 

CO 




vO 

rH 

<N 

O' 

CD 

N* 

m 

m 


vO 


Cl 

CN 

(O 


ro 

o 



O' 

ro 

ro 

fO 

O' 

CN 

rH 



o 

o 

to 

rH 

CO 

in 


m 

m 


CO 

r' 

OJ 

VO 

VD 

(O 

V 

CO 


CO 


CO 

VD 

CO 

fO 

rH 

CO 



O rH 










• 

• 

• 

• 

• 

• 

• 

• 


• 

• 

• 

• 

• 

• 

• 

• 



C fiJ 
(1) > 

m 

tn 

VO 



<n 

o 

CN 


o 

o 

o 

o 

O 

o 

o 

o 


o 

o 

o 

O 

o 

o 

o 

o 
































•H 0) 
MH 4J 

c c 

CO 

r- 


m 

rH 


rH 

r- 


rH 

rH 

00 


CO 

VD 

ro 



rH 

ro 

ro 

r* 

CD 

rH 

tn 

ro 



O -H 

O' 

fO 

O 

VO 

CN 

vO 

CO 

rH 


vO 

O' 

m 

CN 

iH 

r' 

O' 

VD 


CO 

O 

<T> 



CD 

vo 

O' 



o 

m 

o 

o 

tn 

rH 

Cf' 

in 

CO 


r' 

(N 

CO 

VJ* 

CN 

m 

m 

m 



ro 

CO 

V 

rH 

m 

tn 

in 
































1 

<N 

1 

tn 

CO 

i 

VO 

CN 

1 

1 


o 

1 

O 

o 

rH 

rH 

o 

o 

o 


o 

1 

O 

O 

rH 

rH 

o 

o 

o 



«) 

1 o 
























• 





H C 

CO 

dP 

dP 

to 

CO 

CO 

to 

CO 


CO 

dP 

CO 

CO 

CO 

to 

CO 

CO 


to 

CJP 

dP 

CO 

CO 

CO 

to 

CO 



C 
















• 

• 


• 







• 



CF' O 
•H -H 
C/) Mh 

z 


m 

2 

2 

3 

2 

2 


2 

in 

3 

2 

2 

2 

rr 

2 



m 

in 

2 

2 

2 

2 

2 



O 

CD 

m 

<N 

CD 

vO 

vO 

O 

o 


O' 

m 

o 

rH 

CTV 

CN 

o 

m 


«? 

ro 

’O' 

CO 

ro 

ro 


ro 



1 

r-l 

ro 

m 



VO 

CO 

in 


r' 

V 

O' 

O 

VO 

rH 

cn 

in 


CO 

p' 

tn 

rH 

CD 

vD 


CN 



Eh ^ 

CTv 

•H 

rH 

O' 

o 

in 

rH 

rH 


CN 

(O 

o 

CO 

O' 


rH 

tn 


CN 

ro 

rH 

CO 

CN 

UI 

O' 

CO 













• 

• 

• 

• 

• 

• 

• 

• 


• 

• 

* 

• 

• 

• 

• 

• 


m 

W 

rH 

> 

O 

<N 

vN 

o 

rH 

o 

o 

o 


rH 

CN 

CN 

rH 

o 

rH 

rH 

rH 


iH 

CN 

CN 

rH 

rH 

rH 

o 

rH 






























Ui 


ro 

VO 

tn 

O' 


r' 

CN 



CO 

CO 

fO 

rH 

CO 

rH 

O' 

rH 


rH 

in 

ro 

o 

ro 


VD 

CO 





ro 

CH 

CN 


CTl 

vD 


rC 

V 

o 


a 

CO 

tn 

m 


CH 

in 

rH 

V 

O 


(0 

p* 




fO 

O 

o 


fO 

CN 

vD 

O 


H 

o 

o 

pH 

CN 

o 

rH 

o 


rH 

o 

o 

rH 

CN 

o 

O 

o 



O 



• 








• 





• 













O rH 


o 

o 

iH 

CN 

rH 

rH 

CN 


O 

o 

o 

O 

o 

o 

o 

o 


O 

o 

o 

O 

O 

o 

O 

o 



C 











' 









1 

1 





































•H 4) 
<JH 





























f: c 


fO 

o 

O' 

CD 

O' 

vn 





rH 

o 

O' 

rH 

in 

in 


O 

CN 

vo 

CO 

CD 

CN 

vD 

CN 



0 -H 

O' 



r> 

o 

rH 

CN 

CO 


CO 

<o 

(Tl 

Cl 

rH 

o 




O 

rH 

CN 

rH 

(O 

O 

CN 




u 

<n 

r-i 

rH 

r* 

(N 

CN 


fO 


V 

CO 

CTl 

VD 

VD 

CO 

i/) 

ro 


in 

tJ' 

O 

vD 

CD 

01 

M 

CO 

















• 


• 


• 

• 





• 





ro 

1 

VO 


n 

r' 

CN 

iH 

CN 


o 

1 

o 

O 

O 

O 

o 

o 

o 


o 

1 

o 

I 

rH 

1 

O 

1 

O 

1 

O 

1 

O 

1 

o 



<y 

1 o 

























• 

• 



-H C 

to 

dP 

dP 

CO 

to 

CO 

to 

(0 


CO 


to 

CO 

to 

to 

CO 

to 


CO 

dp 

C3P 

to 

to 

to 

to 

(0 



c2 flj 














• 



• 





• 



• 




o> o 

•H 'rl 

CO 'w 

e: 

m 

tn 

2 

2 

2 

2 

2 


2 

m 

2 

2 

3 

2 

2 

2 


2 

tn 

m 

2 

2 

2 

2 

2 



0 

m 


ni 

CD 

VO 

vD 

o 

O 


<7' 

tn 

o 

rH 

O' 

CN 

o 

m 


r? 

CO 


03 

ro 

CO 

rH 

CO 



1 V 


fO 

m 

V 


vO 

CO 

in 



V 

(n 

o 

VO 

rH 

O' 

in 


CO 

r- 

in 

rH 

03 

vo 

-v? 

CN 



£h r-J 

O' 


rH 

O' 

o 

UI 

rH 

rH 


CN 

CO 

a 

CO 



rH 

in 


CN 

ro 

rH 

r -1 

CN 

i/l 

O' 

CO 



<0 

• 

• 

• 


* 

» 

• 

• 


• 

• 

» 

f 

• 

• 

» 

• 


• 

• 

» 

• 

* 

• 

• 

» 



> 

o 

(N 

<N 

o 

rH 

O 

o 

o 


i-H 

<N 

CN 

rH 

o 

rH 

rH 

rH 


rH 

CN 

CN 

rH 

rH 

rH 

o 

rH 






























































fO 

vO 

tn 

O' 

r? 


CN 



CO 

CD 

CO 

rH 

CO 

rH 

CTl 

•H 


rH 

in 

CO 

O 

ro 


vo 

CO 


Ui 



V 

(T) 

CH 

CN 

r* 

O' 

vo 


rH 


o 


CN 

CO 

tn 

tn 


CN 

m 

rH 


O 

'Vf 

CO 




ro 

o 

o 


CD 

CN 

vO 

O 


rH 

O 

o 

rH 

CN 

o 

rH 

o 


rH 

o 

O 

H 

CN 

O 

o 

o 













• 




• 


• 





• 





• 



o r-< 


o 

o 

rH 

CN 

rH 

rH 

CN 


O 

o 

o 

O 

O 

o 

o 

o 


O 

o 

o 

O 

O 

o 

o 

o 



C RI 
<y > 




















1 

1 








•0 U 
H m 
•U 4-> 

c: c 

rH 

n 

o 

O' 

ro 

O' 

vO 





rH 

O 

O' 

rH 

cn 

tn 


o 

CN 

vO 

CO 

CO 

(N 

vo 

CN 



0 ri 

O' 


'4* 


o 


CN 

n> 


CO 

CO 

on 

O 

rH 

o 




o 

rH 

IN 

rH 

to 

O 

CN 




O 

n 

rH 

iH 


n 

CN 

V 

fO 



0) 

O' 

vD 

VD 

O') 

m 

fO 


tn 

(J\ 

O 

VD 

C3 

CO 

CN 

CO 






• 






• 


• 





• 


• 




t 







ro 

t 

vO 

f*' 

rn 


CN 

rH 

CN 


o 

1 

o 

o 

O 

O 

o 

o 

o 


o 

1 

O 

1 

H 

1 

O 

1 

o 

1 

o 

1 

O 

1 

o 






m 

o 

r* 

m 


cn 

vD 

fO 


CN 

O' 



CN 

in 

O' 

CO 


CJ' 


O' 

vo 


CN 

p' 




t/' 


o 

VO 

tn 

vO 

o 


CN 

CO 

CO 

in 

CO 

CN 

CO 

ro 

CN 

(O 

o 

tn 


ro 

V 

VD 

m 



ro 

rH 

O 


n 

r' 

cn 

o 

rH 

in 

CN 

V 

in 

ro 

CO 

(N 

CN 

CN 

O' 

CN 

Ul 

Ul 

ro 

u> 

CN 

rH 

CN 

CO 


U 

(N 


V 

ro 

m 

m 

CN 

»o 

CO 

O 

o 

o 

o 

o 

O 

o 

O 

CN 

O 

o 

o 

o 

O 

o 

O 

O 

CN 











CN 























m 

O 


rn 


m 

VO 

CO 

r* 

CN 

O' 


<3* 

CN 

ul 

O' 

ro 

r> 

O' 


CD 

vD 

P- 

CN 

P* 

c 

4- 

r-l 

U”) 


o 

vO 

in 

vo 

o 


CN 

01 

fO 

m 

m 

CN 

CD 

ri 

CN 

CO 

o 

tn 

r- 

ro 

N* 

vD 

m 



CN 

rH 

O 

r» 

m 


m 

o 

rH 

in 

CN 

V 

in 

CO 

ri 

CN 

CN 

CN 


CN 

in 

in 

ro 

in 

CN 

rH 

CN 

CO 

<D 

U 



V 

m 

m 

m 

CN 

CO 

fO 

O 

o 

o 

O 

O 

O 

O 

O 

CN 

O 

o 

o 

o 

o 

O 

O 

O 

CN 











CN 





















r>» 

in 

a 

m 

m 


o 

O 

rH 

O' 

rH 


cn 

rH 

O' 

'T 

c^ 

O' 

fO 

ro 

o 

p' 

rH 


P- 

O 

CO 



CO 


vO 

CN 

(N 

CO 

O 

m 

rH 

CO 

CN 

CO 

CN 

c^ 

CD 


ro 

VD 


CN 


ro 

CN 

rH 

O' 

CN 

CD 



o 

O' 

rH 

rH 

cn 

CO 

CN 

O' 

r' 

O 

o 

o 

rH 

rH 

o 

o 

o 

VD 

o 

O 

o 

rH 

CN 

rH 

o 

rH 



CO 


o 


CN 


CN 

CN 

CN 

vO 

O 

o 

O 

o 

o 

o 

o 

o 

O 

o 

O 

o 

o 

O 

o 

o 

o 

o 











rH 





















Postenterectomy 
















































■».. r'. 


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DISCUSSION 


In 1955, HarniuGr found 100% mortality in dogs in whom ha had 
resected 80% of the small intestine (1). They were all dead from 
cachexia within ninety days of the enterectomy. The dogs in the present 
study all had a 90% enterectomy, and were pursuing the same downhill 
course as Hammer's dogs. At forty-nine days postenterectomy, or 
approximately one-half the anticipated survival time, an 8 cm. segment 
of their jejunum was reversed, to work in an antiperistaltic way. Ninety 
days after this, the dogs were alive and well, and their body weights 
stable. Although the therapeutic application of this experiment is 
clear, one of the unwanted side effects of the operation was an increase 
in gastric secretion up to 372% of the control value. This hyper¬ 
secretion, the alimentary transit times, and the changes in body 
weight are discussed below, 

I. Increase in Gastric Secretion 

The Heidenhain Pouch hypersecretion following massive enterectomy 
was expected, and the possible mechanisms discussed in Part I of this 
thesis. The further increase of Heidenhain Pouch secretion, both in 
volume and acid concentration, after insertion of the antiperistaltic 
segment, reached statistically significant levels (up to three and 
one-half times the controls) both in the postprandial (p = 0.01) and the 
fasting (p = 0,05) twenty-four hour collections. In a patient-with a 


156 




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157 


reversed segment, acid levels of three and one“half times normal might 
lead to iatrogenic acid peptic disease, and, depending on the proximity 
of the suture line to the parietal cells, stomal ulceration. 

In the eight hours awake collections, the absence of any change 
in Heidenhain Pouch secretion following either enterectomy or reversal 
suggests that random external stimuli which may act to inhibit gastric 
secretion are abrogated during periods of sleep or anaesthesia. The 
same dogs, anaesthetized, showed postenterectomy and postreversal 
changes over the controls of 214% and 267% (postprandial), and 156% 
and 172% (fasting) respectively, in Heidenhain Pouch secretion, though 
none of these changes was statistically significant. 

The proposed causes of this gastric hypersecretion following 
the enterectomy are discussed in Part I of this thesis. The suggested 
cause of gastric hypersecretion following reversal in antral stasis. 
Delayed gastric emptying was produced by inserting the antiperistaltic 
segment close to the pylorus, just beyond the distal end of the duodenum, 
and in several of the barium studies, reflux through the pylorus was 
demonstrated. Pictorial proof of prolonged stimulation of the antrum 
demonstrates a possible explanation of the elevated Heidenhain Pouch 
secretion after segmental reversal. 

II. Increase in Transit Time 

In the normal gastrointestinal tract, the ileo-cecal valve acts 
as a control, causing a delay in transit of the luminal content. Experi¬ 
ments in which the ileo-cecal valve has been bypassed have shown a sub¬ 
sequent intestinal hurry, with absorptive losses (2), In a shortened 



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158 


intestine, the insertion of.an antiperistaltic segment serves the same 
function, naniely to increase the length of time that the foodstuffs are 
in contact v/ith the intestinal absorbing surface, and so produce an in¬ 
creased uptake of nutrients. There is a fine line between a segment 
long enough to affect transit time significantly, and yet short enough 
not to produce a pathological obstruction. The optimum length varies 
according to the site of insertion, generally increasing in length as 
the site becomes more distal, and the absorptive power less (3, 4, 5). 

The aim of the procedure is to promote maximim absorption of nutrients 
from the intestinal tract by prolonging alimentary transit time. 

In our study, the mean gastric emptying time was increased from 
four and one-half to six hours. The delay is demonstrable only proximal 
to the site of the antiperistaltic segment; and when this treatment is 
used therapeutically, the position of insertion will be determined by 
the clinical condition. For example, Poth has constructed pouches 
containing iso- and antiperistaltic components to replace the stomach (6) 
in the treatment of the dumping syndrome, while other surgeons have, v/ith 
some benefit, reversed a segment between stomach and duodenum, or 
immediately distal to the Ligament of Treitz. Postvagotomy diarrhea 
has also responded to this treatment in the hands of some workers (8). 
Should the therapy be to compensate for massive loss of small intestine, 
as in the treatment of mesenteric thrombosis, volvulus, Crohn's disease, 
extensive cancer or trauma, the segment may be placed in such a position 
as to maintain the liominal content in the area where absorption is thought 
to be greatest, for the longest possible time. Investigators have sug¬ 
gested a point about 90 cm. below the Ligament of Treitz as the site of 


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159 


election in man (9). In addition to the weight loss, diarrhea, stea¬ 
torrhea, hypoproteinemia, and hypocalcemia that follows massive enter- 
ectomy, the severe losses of Vitamins B12 and C have proved trouble¬ 
some; and absorption of these elements is usually complete by the first 
100 cm. distal to the Ligament of Treitz. Other investigators have 
noted that in mesenteric artery thromboses, only about 30-40 cm. of 
jejunim survives distal to the Ligament of Treitz, as a result of the 
collateral blood supply from the pancreaticoduodenal artery (7). For 
this reason, their experimental work has used reversed segments at 
about 40 cm. distal to the Legament of Treitz, with favorable results, 
namely the preservation of nutrition and body weight. 

Ill. De cline in Body Weight 

Immediately after enterectomy, the dogs began to lose weight 
at a mean rate of 1 kg. a week, for two weeks, and then more gradually 
at 1 kg. every two v/eeks, for the next six weeks. The rapid early 
weight loss probably represents the additive effects of surgical stress, 
intravenous feeding for several days, and the grossly shortened in¬ 
testinal absorbing surface, while the more gradual later losses indicate 
the purely anenteric element. In support of this conclusion, it was 
found that by the end of two weeks after insertion of the anti- 
peristaltic segment, the effects of the operation were apparent: four 
of the dogs had begun to gain weight slowly, and the steep fall (in the 
two smallest dogs) had been arrested. The mean weights theh levelled 


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160 


The immediate cause of weight loss in the short bowel syndrome is 
probably failure of fat absorption. Although all three main food con¬ 
stituents are less effectively absorbed after enterectomy, investigators 
have shown that fat absorption is more impaired than that of protein or 
carbohydrate (10, 11). The resultant steatorrhea and weight loss has 
been partially compensated by the oral administration of medium chain 

triglycerides (12). Methscopolamine bromide (epoxytropine trooate 

* 

methylbromide ) 2.5 mg. per kg. body weight twice a day has been added 
by Hammer and his associates to the diet of 80% enterectomized dogs, with 
survival, against similarly enterectomized dogs who received no meth- 
scopolamine, which all died. Two of the six dogs receiving methscopo- 
lamine were then taken off it, and also died, while their colleagues 
still receiving the drug all lived (13). 

At the conclusion of our study, the mean body weight of our dogs 
was steady at 75% of their control weight, and the dogs were healthy. 
Autopsy showed the reversed segments to be uncomplicated, and the 
intestine proximal to the segments to be dilated. Some workers have re¬ 
ported a narrowing both in length and breadth of the reversed segment in 
long term follow-up, although its therapeutic function remained unim¬ 
paired, and biopsy was normal (13, 14). Trichobezoar formation in dogs 
has resulted in fatal obstruction when the reversed segment is placed 
near the ileo-cecal valve, possibly exacerbated by the narrowing of the 
segment with time (15). A rare complication in this regard has been the 
formation of bezoars from splinters and wood shavings chewed off wooden 


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161 

cages by the dogs postoperatively, and a clinical precaution after this 
procedure on patients would be to restrict the intake of high residue 
foodstuffs, such as oranges, capable of producing a low obstruction. 





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FOOTNOTES 


^HAMMER, J.M., SEAY, P.H., HILL, E.J., PRUST, F.W,, and 
CAMPBELL, R.B, Intestinal segments as internal pedicle grafts. 

Arch. Surg., 71^; 625-'642, 1955. 

2 

STAHLGREN, L.H., UMANA, G., ROY, R., and DONNELLY, J. ' 

A study of intestinal absorption in dogs following massive small in¬ 
testinal resection and insertion of an antiperistaltic segment. 

Ann. Surg., 156 :483-490, 1962. 

3 

COGSWELL, H.D. Massive resection of the small intestine. 
Ann. Surg., 127:377-382, 1948. 


4 

BORGSTROM, B., et al. Studies of intestinal digestion and 
absorption in the human. J. Clin. Invest., 2^=1521-1536, 1957, 

5 

BALDWIN-PRICE, H.K., COPP, D., and SINGLETON, A.O., Jr. 

Reversed intestinal segments in the management of anenteric malabsorption 
syndrome. Ann. Surg., 161 :225-230, February, 1965. 


6 

POTH, E.J., and CLEVELAND, B.R. A functional substitution 
pouch for the stomach (B). Arch. Surg., 8^:42-54, July, 1961. 

7 

KIMURA, S., and DRAGSTEDT, L.R., II, Reversed 3 e 3 unal segments 
and gastric hypersecretion. Arch. Surg., 98_: 713-715, June, 1969. 

g 

SCHLICKE, C.P. Complications of vagotomy. Amer. J, Surg., 
106:206-216, August, 1963. 

9 . 

FINK, W.J., and OLSON, J.D. The massive bowel resection syn¬ 
drome; treatment with reversed intestinal segments. Arch. Surg., 94 : 
700-706, November, 1966. 

^^SINGLETON, A.O., Jr., KURRUS, F.D., and DONEGAN, D.W. The 
increasing of absorption following massive resections of bowel by means 
of antiperistaltic bowel segments as measured by radioiodine fat abs¬ 
orption studies. Ann. Surg., 154 :(suppl) 130-132, 1961. 












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^\lTHAUSEN, T.L., UYEYAMA, K., and SIMPSON, R.G. Utilisation of 
food from a "natural" versus a "synthetic" diet and a comparison of 
intestinal absorption tests with nutritional balance studies in a 
patient with only 45 cm. of small intestine. Gastroenterology, 12 : 
795-807, 1949. 

12 

WINAWER, S.J., et al. Successful management of massive small 
bov/el resection based on assessment of absorption defects and nutritional 
needs. New Eng. J. Med., 274 ;72-78, 1966, 


^^HARMJ]R, J.L., SEAY, P.H., JOHNSTON, R.L., HILL, E.J., PRUST, F.H., 
and CAMPBELL, R.J. The effect of antiperistaltic bowel segments on 
intestinal emptying time. A.M.A. Arch. Surg., 79_:537-541, 1959. 

14 

MADDING, G.F. Discussion at 74th annual session of the 
Western Surgical Association, Phoenix, Arizona, November 17-19, 1966, 
following presentation of a paper by Fink, J.W,, and Olson, J.D. 

(Ref, 9) . 

^^DRAGSTEDT, L.R. Personal communication. 

^^POTH, E.J. Discussion at 74th annual session of the Western 
Surgical Association, Phoenix, Arizona, November 17-19, 1966, following 
presentation of a paper by Fink, J.W., and Olson, J.D. (Ref. 9). 




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BIBLIOGRAPHY 


\ltHAUSEN, T.L., UYEYAMA, K,, and SIMPSON, R.G. Utilisation 
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intestinal absorption tests with nutritional balance studies in a 
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2 

ANDERSSON, S. Inhibitory effect of hydrochloric acid in 
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3 

ANDERSSON, S. Handbook of Physiology. Am.er. Phys. Soc . , 1967. 

4 

ANDERSSON, S,, NILSSON, G., and UVNAS, B. Inhibition of 
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Acta. Physiol, Scand,, _^:191, 1965. 

5 

BABKIN, B.P. Die aussere Sekretion der Verdauungsdrusen 
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^BALDWIN-PRICE, H.K., COPP, D., and SINGLETON, A.O., Jr, 

Reversed intestinal segments in the management of anenteric mal¬ 
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7 

BAYLISS, W.M, Principles of general physiology (3rd edition), 
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%AYLISS, W.M., and STARLING, E.H. The mechanism of pancreatic 
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M.F. Factors responsible for the intestinal phase of gastric 
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^'^BEAUMONT, W. Experiments and observations on the gastric 
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164 





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165 


12 

BERGSTROM, H., and BROOME, A. Preoperative determination of 
the boundary betv/een the gastric antrum, and fundus. Acta. Clin. 

Scand., 128:526-529, 1964. 

^^BIBLER, D.D., Jr., HARKINS, H.N,.,, and NYHUS, L.M. 

Inhibitory effect of fat in the duodenum and upper small intestine on 
exogenous gastrin stimulated gastric secretion. Surgery, 60, ^-.844- 
847, October, 1966. 

^"^BLACK, J.W., FISHER, E.W. , and SMITH, A.N, The effects of 5- 
Hydroxy-trvptamine on gastric secretion in anesthetized dogs. 

J, Physiol., 141 :27, 1953. 

15 

BLAIR, D.W., and FORREST, A.P.M. Effect of local anti¬ 
histamines on gastric secretion in dogs. Brit. J. Surg,, 47_:425, 1960, 

^^BLONDLOT, N. Sur le principe acide du sue gastrique. 

J. de la physiol, de I'homme, 1^:308-320, Par, 1858, 

17 

BORGSTROM, B., et al. Studies of intestinal digestion and 
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1 q 

BRAASH, J.W., and SEDGWICK, C.E. Reversed loops in the short 
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^^CARD, W.I., and MARKS, J.N. The relationship between the 
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and the parietal cell mass. Clin, Sci,, 1^:147, 1960. 

CARLSON, A.J. The secretion of gastric juice in health and 
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^^CHEY, W,H., and LORBER, S.H. Influence of pancreas on gastric 
secretion in dogs. Am. J, Physiol,, 212(2) :252-260, 1967, 

CHOW, K.Y, Effect of enterectomy on gastric secretion. 

M.Sc, Thesis, University of Alberta, 1968, 

^^CLARKE, J.S,, HOFFS, M,, ELFARRA, S. The effect of portacaval 
transposition on Heidenhain pouch secretion in response to various 
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^^CODE, C.F, Histamine and gastric secretion. In; Histamine. 
Ciba Foundation Symposium, edited by G.E.W, Wolstenholme and C.M, 
O'Connor,, Boston. Little and Brown, 472 :189-219, 1956. 








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25 

COGSWELL, H.D, Massive resection of the small intestine, 
Ann, Surg., 127 ;377-382, 1948. 

26 

COPELAND, E.M., MILLER, L.D., and SMITH, G.P. The complex 
nature of small bowel control of gastric secretion, Ann, Surg., 

168 ;36-45, July, 1968, 

27 , 

DOUTHWAITE, A.H,, and LINTOTT, G.A,M. Gastroscopic 
observation of the effect of aspirin and certain other substances on 
the stomach. Lancet, 235:1222, November, 1938, 


DRAGSTEDT, L.R,, Pathogenesis of gastroduodenal ulcer. 

Arch. Surg,, ^^:438-451, March, 1942, 

29 

DRAGSTEDT, L.R, Gastrin and peptic ulcer. Arch, Surg., 
^:1005-1010, Dec. 1965, 

30 . . 

DRAGSTEDT, L.R. Personal communication, 

31 

DRAGSTEDT, L., WOODWARD, E.R,, STOPvER, E.H., OBERHELMAN, H.A,, 
and SMITH, C,A. Quantitative studies on the mechanism of gastric 
secretion in health and disease, Ann. Surg., 132;626, 1950, 


32 

DRAGSTEDT, L.R., WOODWARD, E.R,, OBERHELMAN, H.A,, STOKER, E.H., 
and SMITH, C.A. Effect of transplantation of antrum of stomach on 
gastric secretion in experiniental animals. Am. J. Physiol., 165 :386- 
398, 1951. 

33 

DRAGSTEDT, L.R., PvAGINS, H,, DRAGSTEDT, L.R., II., and 
EVANS, S.O., Jf. Stress and duodenal ulcer, Ann. Surg,, 144. ; 450, 1956. 

34 

DRAGSTEDT, L.R. II, JOHNSON, A.N. Jr,, SINGER, E.R., and 
OBERHELMAN, H.A. The effect of vagotomy on the intestinal phase of 
gastric secretion. Surg, Forum, ]M;336, 1960. 

35 

DRAPNAS, T,, MCDONALD, J.C., and STEWART, J.D, Serotonin 
release following instillation of hypertonic glucose into the proximal 
intestine. Ann. Surg., 156;528, 1962, 


3 6 

DUVAL, M.K., Jr., and PRICE, W.E. The mechanism of antral 
regulation of gastric secretion; continuous cross circulation, 

Ann. Surg., 152;410, 1960, 











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49 

GREENLEE, H.B., LOUGHI, E.H., GUERRERO, J.D., NELSEN, T.S., 
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53 ' ' 

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54 

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HAMMER, J.M,, SEAY, P.H., HILL, E.J., PRUST, F.W., and 
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CQ 

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S9 

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HOI'IE, C.W., WIGGLESWORTH, W.C,, and PO^-ffiLL, W.J, Gastric 
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G 2 

IRVINE, W,T, The liver, gastric secretion and histamine. 
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63 ' ’ ' 

IRVINE, W.T., DUTHIE, H.L., RITCHIE, H.D,, WATON, N.G. 

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IVY, A.C. A brief review of the physiology of the duodenum. 
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G5 

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170 


75 

LECONTE, P. Cellule. 1^:307, 1900, 

76 

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MENGUY, R, Editorial, Gastroenterology, 51:430-432, 
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8 6 

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87 

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105 , . . , . . , 

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108 ^ ■ I ■ • 

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109 

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Ann. Surg,, 156 ;483-492, 1962, 





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123 

SOKOLOV, A.P,, Thesis, St, Petersburg, 1904. Quoted by 
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WORMSLEY, K.G., MAHONEY, M.P., and NG, M. Effects of a 
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