Potentiation of Mecholyl-Stimulated Gastric Secretion by Hydrocortisone in Heidenhain Pouch Dogs

1958 ◽  
Vol 235 (6) ◽  
pp. 735-736
Author(s):  
DAVID C. H. SUN ◽  
HARRY SHAY
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.


1953 ◽  
Vol 174 (2) ◽  
pp. 219-225 ◽  
Author(s):  
Shirl O. Evans ◽  
Jose M. Zubiran ◽  
Jack D. McCarthy ◽  
Herzl Ragins ◽  
Edward R. Woodward ◽  
...  

1966 ◽  
Vol 1 (2) ◽  
pp. 124-131 ◽  
Author(s):  
M. Mignon ◽  
J.-M. Limbosch ◽  
J. H. Wyllie ◽  
M. J. Rheault ◽  
L. M. Nyhus

1959 ◽  
Vol 196 (6) ◽  
pp. 1262-1265 ◽  
Author(s):  
E. S. Nasset ◽  
V. W. Logan ◽  
M. L. Kelley ◽  
Mary Thomas

Four dogs with Thomas gastric pouches and one dog with a Heidenhain pouch were stimulated to secrete gastric juice by feeding 100 gm of lean beef. Feeding whole desiccated thyroid ordinarily caused a significant fall in volume of gastric juice and in the total quantity of HCl secreted. Crystalline thyroxine yielded erratic results and one trial with triiodothyronine produced a significant increase in gastric secretion. Thyroidectomy in one dog resulted in a gradual decline in secretion, but hypothyroidism produced by administration of mercaptoimidazole in another animal lead to a significant increase in secretion.


1975 ◽  
Vol 228 (6) ◽  
pp. 1775-1781 ◽  
Author(s):  
S Nasca ◽  
M Mignon ◽  
L Gramatica ◽  
J-P Accary ◽  
S Bonfils

Antrocolic transposition in four dogs with Heidenhain pouch and gastrojejunostomyresulted in a marked increase in fasting plasma gastrin concentration and sustained highacid secretion, closely related to gastrin levels. A marked production of pepsin output could not be correlated with plasma gastrin. Reduction in plasma gastrin concentration was more than twofold less pronounced than the reduction in acid output for 1 and 2 U/kg-h, while the 0.5 U/kg-h no effect was noted. For both acid output and gastrin concentrations, close correlations were noted between presecretion level and remaining level upon secretin infusion. Despite the reduction in the secretory volume of the pouch, 0.5 and 1 U/kg-h of secretin induced a 1.5- and 2-fold increase in pepsin output, respectively. Two untis per kilagram-hour decreased the secretory volume as well as the pepsin output. If the physiological release of secretin in dogs does not exceed the equivalent of the lowest dose studied, our results would indicate that acid inhibition is a physiological activity of secretin, while the effect on circulating gastrin concentration seems to be phamacological.


1957 ◽  
Vol 190 (3) ◽  
pp. 396-402 ◽  
Author(s):  
Herbert B. Greenlee ◽  
Enrique H. Longhi ◽  
Jose Delgadillo Guerrero ◽  
Thomas S. Nelsen ◽  
Abdul Latif El-Bedri ◽  
...  

In dogs prepared with both a vagus denervated Heidenhain pouch and a total pancreatic fistula, the intravenous injection of pancreatic secretin (Lilly) produced a profuse secretion of pancreatic juice and a simultaneous marked inhibition of gastric secretion. In dogs prepared with an isolated antrum pouch and a Heidenhain pouch the gastric secretion induced by the instillation of food in the antrum pouch was completely inhibited by the intravenous injection of pancreatic secretin. On the other hand, the intravenous injection of pancreatic secretin had little or no effect on the secretion of gastric juice produced by insulin hypoglycemia or by the injection of histamine. It is suggested that pancreatic secretin may represent the mechanism by means of which acid food in the duodenum inhibits gastric secretion. It is probable that this inhibition is caused by prevention of gastrin release from the antrum rather than to a depressant effect on the parietal cells.


1957 ◽  
Vol 191 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Enrique H. Longhi ◽  
Herbert B. Greenlee ◽  
Jose L. Bravo ◽  
Jose Delgadillo Guerrero ◽  
Lester R. Dragstedt

Acid applied to the antrum mucosa in dogs inhibits the gastric phase of gastric secretion as exhibited in the vagus denervated Heidenhain pouch. To determine if this inhibition of secretion is due to failure of formation or release of gastrin from the antrum, or to the liberation of an inhibitory hormone from the gastric antrum which acts on the parietal cells, dogs were prepared with an isolated Heidenhain pouch and two pouches prepared from the gastric antrum. These antrum pouches were prepared with vagus innervation intact and with vagus innervation eliminated. Gastric secretion in the Heidenhain pouch elicited by the introduction of liver solution or acetylcholine into one of the antrum pouches was not inhibited by the introduction of acid into the second antrum pouch. These data suggest that acid in contact with the antrum mucosa prevents the formation or release of gastrin and does not release an inhibitory hormone.


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