The effect of hog gastrin on gastric secretion in chronic gastric fistula rats

1968 ◽  
Vol 24 (6) ◽  
pp. 563-565 ◽  
Author(s):  
Y. H. Lee ◽  
J. H. Thompson
1989 ◽  
Vol 256 (1) ◽  
pp. R181-R186
Author(s):  
A. Bado ◽  
M. J. Lewin ◽  
M. Dubrasquet

The brain and gut peptide bombesin has been reported both to stimulate gastric secretion and to induce satiety. To understand how the peripheral administration of bombesin affects food intake and whether gastric mechanisms are involved, a comparative study of the doses of bombesin active on gastric secretion, gastric emptying, and food intake was undertaken in cats provided with a gastric fistula and a denervated Heidenhain pouch. The smallest dose of intravenous bombesin that stimulated significantly basal acid secretion (20 pmol.kg-1.h-1) by the gastric fistula also enhanced meal-stimulated acid secretion by the Heidenhain pouch (+138%, P less than 0.01), delayed gastric emptying of a liquid protein meal (-30%, P less than 0.01), and suppressed food intake when the test meal was allowed to reach the stomach (-15%, P less than 0.01). Conversely, in sham-feeding experiments, the same dose of bombesin increased food intake (+35%, P less than 0.01). In full-day experiments conducted in nonfasted cats, bombesin decreased both the food intake in the 4-h period after the infusion and the daily food intake, whereas octapeptide cholecystokinin induced a transient satiety but did not decrease daily food intake. These results indicate that in cats the interaction of bombesin with "pregastric" mechanisms is not sufficient to induce satiety and that a relation could exist between the effects of bombesin on gastric secretion, emptying, and food intake. A single class of receptors might be involved in these peripheral effects of bombesin.


1965 ◽  
Vol 209 (2) ◽  
pp. 319-323 ◽  
Author(s):  
Peter T. Ridley ◽  
Frank P. Brooks

Fasting gastric secretion and secretion during insulin hypoglycemia were collected from hypothalamic hyperphagic rats equipped with chronic gastric fistula in an attempt to correlate the hypothalamic neural mechanisms controlling food intake with gastric secretion. The interdigestive or basal fasting secretion of rats rendered hyperphagic by stereotaxic ablation of the ventromedial nuclei was significantly increased in volume, acid concentration and output, and pepsin output when compared with control and sham-operated rats and rats with hypothalamic lesions without hyperphagia. Hypothalamic hyperphagic rats did not show a significant increase in gastric secretion during insulin hypoglycemia, whereas the other groups did. The levels of hypoglycemia induced by insulin were comparable in all groups. These studies suggest an important role of the ventromedial nuclei in the central regulation of acid and pepsin secretion, and also relate the hypothalamic neural control of gastric secretion to that of food intake. The results also indicate that this nucleus is involved either as a "center" or pathway in the augmentation of gastric secretion by insulin hypoglycemia.


1957 ◽  
Vol 190 (2) ◽  
pp. 221-228 ◽  
Author(s):  
Ardelle Lane ◽  
A. C. Ivy ◽  
Emma K. Ivy

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.


1957 ◽  
Vol 191 (2) ◽  
pp. 262-264 ◽  
Author(s):  
Ardelle Lane ◽  
A. C. Ivy ◽  
E. K. Ivy

It was found in four tests on each of 12 rats with a chronic gastric fistula and accustomed to the experimental procedures that insulin hypoglycemia short of convulsions stimulated gastric secretion when the vagus nerves were intact. In five tests on each of seven rats, it was found that section of the vagi abolished the secretory response to insulin hypoglycemia. This evidence is interpreted as establishing the presence of gastric secretory nerves in the vagi of the rat.


1963 ◽  
Vol 205 (2) ◽  
pp. 230-234 ◽  
Author(s):  
S. A. Komarov ◽  
S. P. Bralow ◽  
H. Shay ◽  
E. Boyd

Variations in several parameters of basal gastric secretion and in the behavior index determined in arbitrary rank units were studied in three groups of rats with chronic gastric fistula. There was an impressive similarity between the groups particularly in the patterns of variation during the 6 hr of observation. Volume and outputs of acid, pepsin, and chloride tended to decrease; a negative linear regression on hours was always significant but significant concave up parabolas often better fitted the data. Concentrations of acid and chloride increased significantly during an average experiment either linearly or in conformity with concave down parabolas. Lower concentrations of acid and chloride occurred concomitant with increases in volume and were considered due to salivary contamination associated with a higher behavior index. All above variations in secretion exhibited a significant linear correlation with variations in behavior index. Pepsin concentrations tended to decrease but were not significantly associated with behavior index. As a rule, there were significant differences among animals within groups, but none among the means of replicate experiments.


1987 ◽  
Vol 73 (1) ◽  
pp. 25-30
Author(s):  
E. P. Dewar ◽  
N. S. Williams ◽  
M. F. Dixon ◽  
D. Johnston

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.


1957 ◽  
Vol 189 (2) ◽  
pp. 369-372 ◽  
Author(s):  
Richard W. Schayer ◽  
A. C. Ivy

One test on each of six chronic gastric fistula rats was made in which after a 12-hour fast C14 l-histidine was injected subcutaneously. Twenty-four hours later, while still fasting, aminoguanidine HCl (AG) (2 mg of the base), a powerful diamine oxidase inhibitor (an antihistaminase), was given hourly subcutaneously through an indwelling needle day and night for 3 additional days. Twenty-four hours after the start of AG, food was given for 12 hours; fasting then occurred for two 12-hour periods, and then food was given again for 12 hours. The average urinary C14 histamine counts per minute during the various AG periods were: first AG control period, 105; second AG control period, 104; 12-hour feeding period, 185; first 12-hour postfeeding-fasting period, 157; second postfeeding-fasting period, 68; final 12-hour feeding period, 106. It is concluded that, on feeding, C14 histamine was released in quantities adequate to stimulate gastric secretion when aminoguanidine was present to prevent histamine destruction.


1964 ◽  
Vol 206 (6) ◽  
pp. 1309-1314 ◽  
Author(s):  
S. P. Bralow ◽  
S. A. Komarov ◽  
H. Shay

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.


1990 ◽  
Vol 258 (6) ◽  
pp. G919-G925 ◽  
Author(s):  
B. I. Hirschowitz ◽  
J. Fong

In four gastric-fistula dogs, selective antral vagotomy markedly reduced the vagal stimulation of gastrin release, thereby defining both the vagal pathway for stimulation of gastrin and the anatomic source of such gastrin release. Despite loss of gastrin response, vagal excitation by 100 mg/kg 2-deoxy-D-glucose (2-DG) produced the same acid and pepsin responses after antral vagotomy as before, but there was an approximately 40% diminished fundic response to pentagastrin, histamine, and synthetic human gastrin, as well as to endogenous gastrin released by graded doses of bombesin. Bethanechol did not reverse the defect, ruling out inadvertent fundic vagal denervation, nor did raising serum gastrin by bombesin alter the response to vagal stimulation by 2-DG. Fundic response to bethanechol was increased by approximately 60%, and the output of gastrin increased at least fivefold after antral vagotomy. Gastrin responses to food were diminished and those to sham feeding were eliminated. Separation of the denervated antral pouch had no additional effect on acid secretion. Vagal stimulation of gastric secretion thus occurs almost exclusively through direct cholinergic effects on the fundus with little or no contribution from antral gastrin. Vagal denervation sensitizes the antrum to cholinergic stimulation.


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