Inhibition Of Pentagastrin-stimulated Gastric Secretion Research Articles

Effect of adding albumin to solutions of somatostatin on inhibiting pentagastrin-stimulated acid secretion in dogs.

In five conscious dogs with chronic gastric fistulas we studied the effect of somatostatin solutions on pentagastrin-stimulated acid secretion. Somatostatin was dissolved in 0.154 M NaCl alone or in the same amount of saline to which dog albumin had been added to give a 0.5% solution. Somatostatin produced a dose-dependent inhibition of pentagastrin-stimulated gastric secretion. However, the inhibition was significantly less when somatostatin was dissolved in saline as compared to saline plus albumin. This study suggests that albumin should be added to somatostatin solutions to preserve biological activity, and it confirms previous reports indicating that, without albumin, basic peptides have a tendency to stick to infusion systems.

SMOKING IMPAIRS THERAPEUTIC GASTRIC INHIBITION

Cigarette smoking reversed the inhibition of nocturnal gastric secretion produced by the H 2-receptor antagonists cimetidine and ranitidine and by the phenothiazine derivative LM 24056. As a consequence of smoking, nocturnal secretion of acid increased by 91·5% and of pepsin by an average of 59% when compared with control studies when patients did not smoke. The inhibition of pentagastrin-stimulated gastric secretion produced by cimetidine or poldine was not affected by cigarette smoking. Since control of nocturnal secretion may be important in promoting ulcer healing and maintenance of remission, patients receiving antisecretory drugs should be advised not to smoke after having taken their nocturnal dose of the drug.

Relationship between hydrogen ion concentration and flow of gastric juice during inhibition of gastric secretion in the cat.

1. The normal relationship between the [H+] and rate of flow of gastric juice was determined in conscious cats prepared with cannulated gastric fistulae. Gastric secretion was monitored during stimulation with pentagastrin, insulin and histamine. 2. [H+] rose asymptotically with the flow of gastric juice. This relationship was quantified by applying the data to the integrated form of the Fick equation for diffusion, a graphical plot of log [H+] vs. 1/flow. The calculated relationships were similar for gastric secretion stimulated by pentagastrin, insulin and histamine, and were used to define the normal relationship between gastric [H+] and flow. 3. Significant inhibition of pentagastrin-stimulated gastric secretion with the histamine H2-receptor antagonists, metiamide and cimetidine, atropine or somatostatin did not alter the normal relationship between [H+] and flow; the [H+] observed fell within the normal range observed at that flow rate in the presence of pentagastrin alone. Similarly, inhibition of insulin-stimulated secretion with metiamide, did not alter the normal relationship between [H+] and flow of gastric juice. 4. These data provide evidence that histamine H2-receptor antagonists, atropine and somatostatin all act to reduce the primary rate of acid secretion and do not influence the [H+] per se, either by interfering with back-diffusion of H+, or by changing the proportions of a non-parietal component of gastric secretion added to the parietal H+ component.

Vasoactive intestinal peptide-associated inhibition of stimulated gastric secretion: II. Inhibition of pentagastrin-stimulated gastric secretion

The possible role of vasoactive intestinal peptide as an inhibitor of stimulated gastric secretion was investigated. Awake dogs with Heidenhain pouches were stimulated with pentagastrin alone and in combination with intraduodenal instillation of various potential inhibitors of gastrointestinal secretion including isotonic phenylalanine, 3 percent hypertonic saline solution and 0.16 normal hydrochloric acid. Plasma vasoactive intestinal peptide is significantly increased by pentagastrin, and this release is enhanced by intraduodenal hydrochloric acid. Simultaneously, there is significant inhibition of pentagastrin-stimulated Heidenhain pouch secretion. These findings provide evidence for a possible physiologic role of vasoactive intestinal peptide as an inhibitor of gastric secretion, at least in dogs.

Release of gastric inhibitor from the intestine of dogs infused intravenously with sodium oleate.

We found previously that intravenous infusion of sodium oleate induced inhibition of pentagastrin-stimulated gastric secretion in canine Heidenhain pouches. In the present study we attempted to verify the hypothesis that such intravenous infusion provoked Extract of intestinal mucosa release, from intestinal mucosa, of an enterogastrone-like inhibitor. Lyophilized extracts of canine intestinal secretion or mucosa were prepared using dogs infused for 6 h with saline or with sodium oleate. These extracts weren then assayed for their inhibitory action by intravenous infusion into Heidenhain pouches of dogs, stimulated with pentagastrin. When solvent or extracts prepared from intestinal juice or gut mucosa of dogs infused with saline were tested, no inhibition of gastric acid occurred. When extracts prepared from dogs infused with oleate were assayed, gastric acid secretion was inhibited. We concluded that intravenous infusion of fat results in the release of a gastric inhibitor of intestinal origin which behaves as an enterogastrone. This may be a most reasonable explanation of the action of intravenous sodium oleate on gastric secretion.

Inhibition of pentagastrin-stimulated gastric secretion by duodenal acidification or administration of fat in normal subjects and in patients with duodenal ulcer

The inhibitory effect of duodenal acidification and intraduodenal fat infusion on pentagastrin-stimulated gastric secretion in normal subjects and in patients with duodenal ulcer was studied. Intraduodenal infusion of acid resulted in inhibition of HCl secretion found to be significant only in ulcer patients. Pepsin output, although lower during the first 15 minutes of duodenal acidification, later increased. Intraduodenal infusion of olive oil resulted in significant inhibition of HCl and pepsin output in both groups of patients, which was maximal 45–60 minutes after the beginning of fat infusion. Gastric secretion was more readily inhibited in ulcer patients than in normal subjects; this difference was particularly evident in inhibition of pepsin secretion. In addition, decrease in concentration of HCl and pepsin was observed to be significant only in ulcer patients. Mechanisms by which duodenal acidification and fat inhibit gastric secretion are discussed. The results obtained suggest that secretin, which is probably responsible for inhibition after duodenal acidification, is not the inhibitor during inhibition by fat. The ulcer patients were found to have unimpaired mechanisms of inhibition by acid and fat.