Effect of total adrenalectomy on gastric secretion in chronic gastric fistula rats

1964 ◽  
Vol 206 (6) ◽  
pp. 1309-1314 ◽  
Author(s):  
S. P. Bralow ◽  
S. A. Komarov ◽  
H. Shay
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Free Acid ◽  
Acid Output ◽  
Cell Mass ◽  
Chloride Concentration ◽  
Sham Operation ◽  
Gastric Fistula ◽  
Total Acid ◽  
Total Chloride

Basal gastric secretion of rats with chronic fistulas was studied before and after adrenalectomy or sham operation. A marked exponential fall in concentration and output of free and total acid resulted in virtual anacidity within 3–7 weeks following adrenalectomy. Failure in parietal cell secretion was not accompanied by significant decrease in parietal cell mass. Pepsin concentration and output as well as volume also fell exponentially but more gradually. No significant change in total chloride concentration occurred. Relative influence of concentration in determining output was 30 times greater than volume for free acid, 3 times greater for total acid, and twice as great for pepsin. Volume was responsible for almost all variability in total chloride output. Time after adrenalectomy influenced variability of volume and acid output twice as much as concurrent decrease in body weight.

Effect of restraint on gastric acidity in the rat

1962 ◽  
Vol 202 (4) ◽  
pp. 812-814 ◽  
Author(s):  
David A. Brodie ◽  
Richard W. Marshall ◽  
Oscar M. Moreno
Keyword(s):  
Gastric Secretion ◽  
Acid Concentration ◽  
Gastric Content ◽  
Free Acid ◽  
Acid Output ◽  
Important Change ◽  
Gastric Fistula ◽  
Total Acid ◽  
Chronic Fistula ◽  
Collection Period

Chronic gastric fistula rats were prepared by implanting stainless steel cannulas in the rumen portion of the stomachs of male Holtzman rats and gastric content was collected in both the unrestrained and restrained state. Gastric secretion in acute pylorus-ligated rats, unrestrained and restrained, was studied at the same time. Volume of gastric content, free and total acidity, and free acid output were significantly lower in the chronic fistula rats as compared to the pylorus-ligated rats in the initial 4-hr collection period. A study of 24-hr gastric content in chronic fistula rats showed that restraint produced a significant decrease in volume, a significant increase in free and total acid concentration, and no change in free acid output, while the restrained pylorus-ligated rats had a significant decrease in volume, no change in free or total acid concentration, and a significant decrease in free acid output as compared with control values. This suggests that an increase in acid concentration is an important change produced in gastric secretion by restraint stress.

Effects of KCl and insulin on benzimidazole-inhibited canine gastric secretion

1983 ◽  
Vol 245 (6) ◽  
pp. G739-G744
Author(s):  
B. I. Hirschowitz ◽  
J. Fong
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Acid Output ◽  
Gastric Fistula ◽  
Large Decrease ◽  
Pepsin Secretion ◽  
K Secretion ◽  
Inhibited Acid ◽  
K Concentration ◽  
Bethanechol Chloride

The final step in acid secretion is believed to result from the H+-K+-ATPase-mediated exchange of H+ in the parietal cell, with K+ in the lumen. To study the K+ secretion we used Picoprazole and insulin separately and together to inhibit gastric secretion stimulated in gastric fistula dogs with histamine (100 micrograms X kg-1 X h-1). Picoprazole, a substituted benzimidazole (750 mg/kg), reduced gastric H+ concentration and volume with a rise in K+ concentration [( K+]) to 20–25 meq/l. Insulin alone inhibited acid output to the same extent as Picoprazole but with a marked fall in [K+]. Insulin (0.6 U/kg) given with Picoprazole did not alter inhibition of H+ but prevented the large decrease in gastric juice [K+]. An injection of KCl (1 meq/kg) 1 h after Picoprazole did not alter the effects of the inhibitor. Pepsin secretion after insulin was delayed by Picoprazole, whereas during bethanechol chloride infusion (80 micrograms X kg-1 X h-1) pepsin output was reduced for a shorter period and to a lesser extent than acid. We concluded that insulin affects gastric H+ and K+ secretion by a mechanism not related to H+-K+-ATPase and that Picoprazole affects pepsin secretion probably indirectly via its effect on the parietal cell, where its action is quite consistent with an effect limited to inhibition of the H+-K+-ATPase of the parietal cell.

Augmented vagal release of antral gastrin by 2-deoxyglucose after fundic vagotomy in dogs.

1979 ◽  
Vol 236 (2) ◽  
pp. E173
Author(s):  
B I Hirschowitz ◽  
R G Gibson
Keyword(s):  
Intravenous Injection ◽  
Serum Gastrin ◽  
Acid Output ◽  
Cholinergic Receptors ◽  
Gastric Fistula ◽  
Gastrin Release ◽  
Total Acid ◽  
Muscarinic Cholinergic Receptors ◽  
Single Intravenous Injection ◽  
Muscarinic Cholinergic

To study the relation between gastrin released by vagal excitation and the secretion of H+ and pepsin under various conditions, central vagal excitation was induced by 2-deoxyglucose (2DG) in doses of 50, 100, and 200 mg/kg body wt given as a single intravenous injection in seven gastric fistula dogs, three with fundic vagotomy and four with intact vagi. Serum gastrin increased linearly with dose doubling in both groups but was twice as high in the vagotomized dogs. Total acid output for 3 h was related linearly to integrated gastrin output in both groups, but the slope, H+/gastrin, was 10 times steeper in the vagally intact dogs (330 vs. 34 mueq/pg gastrin-ml-30 min) and pepsin output almost 20 times greater [5,400 peptic units (PU) vs. 296 PU]. Acidification of the antrum to pH 1.2-1.4 eliminated the gastrin response to 2DG in both groups of dogs. Atropine (100 microgram/kg iv) reduced serum gastrin in the vagotomized and increased it in the intact dogs. Atropinization uncovers stimulation by 2DG by pathways that do not involve muscarinic cholinergic receptors. Stimulation by both pathways is suppressible by acid. We conclude that fundic vagotomy removes an inhibitor of vagal gastrin release.

The Relation between Functioning Parietal Cell and Gastrin Cell Masses in Two Groups of Duodenal Ulcer Patients

1976 ◽  
Vol 50 (5) ◽  
pp. 375-383 ◽  
Author(s):  
D. J. Byrnes ◽  
Shiu Kum Lam ◽  
W. Sircus
Keyword(s):  
Duodenal Ulcer ◽  
Parietal Cell ◽  
Serum Gastrin ◽  
Acid Output ◽  
Ulcer Patient ◽  
Cell Mass ◽  
Inverse Correlation ◽  
Normal Subjects ◽  
Gastrin Cell ◽  
Before And After

1. Serum gastrin concentrations before and after a standardized meal were determined in twenty-eight patients with duodenal ulcer and in ten normal control subjects. 2. In response to pentagastrin, thirteen of the duodenal ulcer subjects secreted acid within the limits of normal and fifteen secreted in excess. 3. The differences in the basal serum gastrin concentrations between the three groups, normal subjects, acid ‘normosecretors’ and hypersecretors were not statistically significant but that of the hypersecretors was suggestively low. 4. The integrated gastrin response and peak gastrin responses to meals were higher in duodenal ulcer patients with normal acid secretion than in the hypersecretors but the values for the latter were not different from normal subjects. 5. Stabilization of intragastric pH by infusion into the antrum of sodium bicarbonate during the test meal response period did not alter these differences between the two ulcer patient groups. 6. A significant inverse correlation exists between the maximal acid output and the integrated gastrin response in both normal subjects and hypersecreting duodenal ulcer patients. 7. The evidence (a) supports the existence of an inverse relationship between the functioning parietal cell and gastrin cell masses, (b) shows the gastrin response in normosecreting ulcer subjects to be inappropriately high, and (c) suggests that excessive vagotonia exerts trophic effects upon both parietal cell mass and gastrin cell mass.

Response of the Chronic Gastric Fistula Rat to Histamine

1957 ◽  
Vol 190 (2) ◽  
pp. 221-228 ◽  
Author(s):  
Ardelle Lane ◽  
A. C. Ivy ◽  
Emma K. Ivy
Keyword(s):  
Body Weight ◽  
Gastric Secretion ◽  
Free Acid ◽  
The Body ◽  
Threshold Dose ◽  
Maximum Output ◽  
Gastric Fistula ◽  
Average Maximum ◽  
Pharmacological Studies ◽  
Control Output

The preparation of chronic gastric fistula rats, their care and how they may be used for physiological and pharmacological studies on gastric secretion is described. The rat has a large interdigestive secretion and secretes free acid (pH 4.5) after 48–72 hours of fasting. For controlled studies this requires the replacement of fluid and chlorides. Statistically significant differences between the control output of acid and the response to 1 mg of histamine diphosphate were obtained. The threshold dose of the diphosphate is approximately 0.1 for a 350-gm rat. The least amount of histamine diphosphate to yield an average maximum output of acid (10 mg/hr.) is 0.5 mg subcutaneously every 15 minutes. The body dose of histamine required to stimulate gastric secretion is about the same in man, dog, cat and the rat. On the basis of body weight, the amount of histamine base required to yield a maximum output of acid in the rat is 34.6 µg/kg/min. as compared with 1.6 µg/kg/min. in the dog.

Cephalic Phase of Gastric Secretion in the Rat

1957 ◽  
Vol 192 (1) ◽  
pp. 23-26 ◽  
Author(s):  
T. M. Lin ◽  
R. S. Alphin
Keyword(s):  
Gastric Secretion ◽  
Gastric Juice ◽  
Free Acid ◽  
Acid Output ◽  
Esophageal Fistula ◽  
Depressing Effect ◽  
Gastric Glands ◽  
Sham Feeding ◽  
Cephalic Phase ◽  
Bilateral Vagotomy

Nineteen sham-feeding tests were performed on eleven rats with a chronic gastric and esophageal fistula. As compared with man and the dog, a slight increase in acid output occurred in 17 tests, the increase being quite definite in 13 tests. Sham feeding had no effect on gastric secretion in 16 tests on rats when performed from 1 to 14 days after bilateral vagotomy. The vagotomy had a profound depressing effect on the interdigestive secretion, no free acid being found in the fasting secretion in any of the rats during the period of these tests. The vagi exert a marked secretory tone on the gastric glands, but the conditioned secretion of gastric juice is probably not of much physiological significance in the rats studied in these tests.

Vagotomy confined to the acid-secreting mucosa of the stomach

1987 ◽  
Vol 73 (1) ◽  
pp. 25-30
Author(s):  
E. P. Dewar ◽  
N. S. Williams ◽  
M. F. Dixon ◽  
D. Johnston
Keyword(s):  
Gastric Secretion ◽  
Myenteric Plexus ◽  
Acid Output ◽  
Gastric Wall ◽  
Neural Tissue ◽  
Gastric Fistula ◽  
Gastric Acid Output ◽  
Before And After ◽  
Acid Secreting ◽  
Gastric Musculature

AbstractChemoneurolysis, using varying concentrations of ethyl alcohol, was performed in dogs with a total gastric fistula in an attempt to denervate selectively only the acid-secreting mucosa, leaving the muscle innervated. Tests of gastric secretion and histological examination of gastric wall biopsies were performed both before and after chemoneurolysis. Chemoneurolysis resulted in a significant reduction in the number of parasympathetic fibres in the submucosa (p<0.01) and a decrease in insulin and pentagastrin stimulated acid secretion. The appearances of the myenteric plexus and gastric musculature were unchanged. The destruction of the submucosal neural tissue was, however, insufficient to produce a th erapeutically significant decrease in gastric acid output.

Preparation of chronic denervated gastric pouches in the rat

1959 ◽  
Vol 197 (2) ◽  
pp. 257-259 ◽  
Author(s):  
R. S. Alphin ◽  
T. M. Lin
Keyword(s):  
Free Acid ◽  
Acid Output ◽  
Gastric Pouch ◽  
Volume Flow ◽  
Gastric Fistula ◽  
Rat Stomach ◽  
Basal Secretion ◽  
Dog Food ◽  
Surgical Preparation

A method is described for the surgical preparation, feeding and care of a chronic denervated gastric pouch in the rat. The basal secretion of the denervated pouch is approximately 0.24 ml/hr. and the hourly free HCl output is nearly zero after a fast of 12 hours. The volume of secretion and the free HCl output both increased after feeding with 3–5 gm of canned dog food. Insulin, 0.5 u, stimulated the output of free HCl from the innervated total gastric fistula but failed to stimulate the volume flow or the acid output of the denervated pouch. A denervated pouch prepared from the squamous or nonglandular portion of the stomach was also described. This portion of the stomach never secreted any free acid at any time over a period of 6 months postoperatively. This is the first physiologic proof that the white portion of the rat stomach is nonacid secreting. The advantages of using a denervated gastric pouch for physiologic and pharmacologic studies are discussed.

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