Effect of somatostatin on histamine-stimulated gastric acid and pepsin secretion in dogs

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and pepsin secretion in conscious dogs with gastric fistula. Infusion of histamine stimulated dose-dependently the acid secretion, whereas pepsin secretion was decreased by the high doses of histamine. Somatostatin inhibited dose-dependently the stimulated acid secretion but only with a maximum of 40%. The pepsin secretion was inhibited by somatostatin dose-dependently and with a higher potency. The acid inhibition was of a competitive type and prostaglandin-independent.     

Effect of serotonin on pentagastrin-stimulated gastric pepsin secretion in dogs with gastric fistula

The effect of serotonin on pentagastrin-stimulated gastric pepsin secretion in dogs was evaluated with regard to dose-response kinetics and receptor mediation. The pepsin secretion showed a dual response to exogenous serotonin. The high and low doses of serotonin stimulated, whereas the doses in between inhibited. The inhibition was of a non-competitive type and could be significantly counteracted by beta-adrenergic blocking drugs. This study supports the concept that the serotonin effect on gastric functions is mediated via sympathetic nerves releasing noradrenaline.     

Effect of serotonin on bethanechol-stimulated gastric pepsin secretion in dogs

The effect of serotonin on bethanechol-stimulated gastric pepsin secretion was evaluated with regard to dose-response kinetics and receptor mediation. A low dose of exogenous serotonin produced a stimulation (0.5 microgram/kg/min), whereas inhibition was found for higher doses (5-10 micrograms/kg/min). The inhibition was non-competitive and could be significantly counteracted by beta-adrenergic blocking drugs. This study confirms results obtained during pentagastrin stimulation and supports the concept that serotonin acts via sympathetic nerves to release noradrenaline.     

Effect of somatostatin on bethanechol-stimulated gastric pepsin secretion in gastric fistula dogs

The effect of somatostatin on pepsin secretion was determined in six dogs with gastric fistulas during stimulation with bethanechol. Somatostatin inhibited dose-dependently the stimulated pepsin secretion, with a dose of 0.3 micrograms/kg/h being 35% inhibitory during stimulation with bethanechol, 80 micrograms/kg/h. Continuous infusion of somatostatin for 3 h did not cause any signs of tachyphylaxis. Withdrawal of somatostatin produced a return to the control level. The dose-response kinetics with five doses of bethanechol with and without somatostatin showed inhibition of a noncompetitive type. The effects of somatostatin were not altered by using adrenergic, dopaminergic, or serotonergic blocking drugs.     

Exogenous serotonin and histamine-stimulated gastric acid and pepsin secretion in dogs

The effects of serotonin on histamine-stimulated gastric acid and pepsin secretion were evaluated in conscious dogs with a gastric fistula. Histamine stimulated the acid secretion dose-dependently, whereas pepsin secretion was decreased by the high doses of histamine. The acid secretion was inhibited slightly by serotonin, with a maximum of 42% with a dose of 10 micrograms/kg/min. The pepsin secretion was only decreased non-significantly by serotonin, 10-15 micrograms/kg/min. The acid inhibition was counteracted by beta-adrenergic antagonists (propranolol, atenolol) and methysergide (serotonergic antagonist). The dose-response analysis showed inhibition of a competitive type. In conclusion, serotonin inhibits histamine-stimulated gastric acid secretion via serotonergic receptors and beta-adrenoceptors, whereas pepsin secretion is unaffected.     

Beta-adrenergic agonists inhibit gastric acid and pepsin secretion through somatostatin release in dogs

The purpose of the present study was to evaluate whether the inhibitory effects of beta-adrenergic agonists on gastric secretory activity in vivo could be mediated through a local release of somatostatin. The gastric secretion was measured during continuous stimulation with pentagastrin (1 microgram/kg/h). The infusion of isoprenaline (beta 1 + beta 2), salmefamol (beta 2), and somatostatin produced inhibitory effects on both acid and pepsin secretion. The reaction patterns were similar for isoprenaline and somatostatin, whereas salmefamol induced an inhibition of longer duration and with dissimilar dose-response kinetics. The gastric somatostatin release was significantly increased after infusion of both beta-adrenergic agonists and somatostatin, with patterns similar to those obtained for the secretory inhibition. There was a significant correlation between the somatostatin release and the acid and pepsin secretion during infusion of the secretory inhibitors but not in the control state. This study shows that beta-adrenergic agonists have inhibitory effects on gastric secretion in vivo similar to those of somatostatin. Both somatostatin and the beta-adrenergic agonists stimulated the release of somatostatin from the gastric mucosa. beta-Adrenergic antagonists were without effects. Somatostatin thereby fulfils the requirements for an endogenous mediator of the beta-adrenergic inhibition.     

Effect of isoprenaline on pentagastrin-stimulated gastric acid secretion in dogs with gastric fistula

The purpose of this study was to elucidate the effect of a beta 1-adrenoceptor agonist on gastric acid secretion in conscious dogs with gastric fistula. Isoprenaline, a beta 1- and beta 2-agonist was used alone and in conjunction with selective blockade of beta 2- and beta 1-receptors. Isoprenaline dose-dependently inhibited the secretory volume and the acidity. The antisecretory effect of isoprenaline was significantly blocked by the beta 1-adrenoceptor blocker practolol and by the beta 1 + beta 2-adrenoceptor blocker propranolol but not by H 35/25, a beta 2-adrenoceptor blocker. This indicates that isoprenaline acts on the acid secretion exclusively through beta 1-receptors. Dose-response experiments with five logarithmically increased doses of pentagastrin and one dose of isoprenaline showed unchanged calculated maximum response and an increase in half-maximum acid response. It is concluded that the inhibitory effect of isoprenaline on gastric acid secretion is of competitive or uncompetitive type.     

The effect of enterectomy on gastric secretion in dogs with biliary fistulas

Bile was excluded from the gastrointestinal tract of 5 dogs with Heidenhain pouches by total external biliary fistulas. After a major portion of the jejunum and the ileum was resected Heidenhain pouch secretions increased in all instances. The results indicate that the increase in gastric secretion which regularly follows small-bowel resection is independent of the presence or absence of bile in the gastrointestinal tract.Supported by Grant AM-7750 from the US Public Health Service.The opinions expressed in this publication are those of the authors and not necessarily those of the US Air Force Medical Service.     

Somatostatin increases the ratio between gastric mucosal blood flow and gastric acid and pepsin secretion in dogs

The effects of somatostatin on gastric mucosal blood flow (GMBF), acid secretion, and pepsin secretion were evaluated. Conscious gastric fistula dogs were used, with neutral red clearance as the method for estimating the mucosal blood flow. Somatostatin inhibited the pentagastrin- and bethanechol-stimulated gastric acid and pepsin secretion and resulted in an absolute decrease in mucosal blood flow. The ratios between GMBF and secretion (acid and pepsin) were increased during somatostatin infusion, which suggests a relative increase in mucosal blood flow and independent inhibition of gastric secretion. It may be concluded from this study that the acid- and pepsin-inhibitory effects of somatostatin are not mediated by changes in the GMBF.     

Effect of somatostatin on pentagastrin-stimulated gastric acid secretion and gastric antral motility in dogs with gastric fistula

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of pentagastrin induced motility with a digestive pattern. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using alpha- and beta-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with seven doses of pentagastrin with and without somatostatin showed inhibition of a competitive type for gastric acid secretion and of a non-competitive type for antral motility with regard to amplitude.     

Effect of serotonin on pentagastrin-stimulated gastric acid secretion and gastric antral motility in dogs with gastric fistula

The effects of exogenous serotonin on pentagastrin-stimulated gastric acid secretion and antral motility were evaluated with regard to inhibition kinetics and receptor mediation. Conscious gastric fistula dogs were used. Serotonin inhibited the acid secretion dose-dependently, whereas the antral motility was initially stimulated and thereafter inhibited. The inhibition of secretion was counteracted by different beta-adrenergic blocking drugs and methysergide, whereas the inhibition of antral motility was blocked by methysergide and indomethacin. Dose-response analysis showed inhibition of non-competitive types. This study supports the concept of differences in the regulation of gastric acid secretion and motility, but further experiments with simultaneous registration are required.     

Effect of somatostatin on bethanechol-stimulated gastric acid secretion and gastric antral motility in dogs with gastric fistula

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of bethanechol stimulated dose-dependently acid secretion, whereas the frequency and strength of antral motility was maintained at a high level. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using alpha-adrenergic, beta-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with four doses of bethanechol with and without somatostatin showed inhibition of a non-competitive type for gastric acid secretion and of a competitive type for antral motility with regard to amplitude.     

Effect of omeprazole on the secretion of intrinsic factor, gastric acid and pepsin in man.

The effect of an intravenous infusion of omeprazole (0.35 mg/kg) and placebo on basal and stimulated (pentagastrin 1.0 microgram/kg/h) secretion of gastric acid, intrinsic factor and pepsin was studied in 10 healthy male subjects. Omeprazole caused a marked inhibition of basal and stimulated acid output. The inhibition of pepsin output was less marked, but also significant. The output of intrinsic factor, however, showed no significant change. The results indicate that acid and intrinsic factor might have different secretory mechanisms within the parietal cell.     

Effect of bulbar perfusion with acid, hypertonic solutions, and acetylcholine on gastric acid secretion in dogs.

Dogs were provided with innervated pouches of the fundic stomach and the duodenal bulb. One dog also had an isolated pouch of the distal duodenum. Acid secretion was stimulated by intravenous infusion of a low dose of pentagastrin (ICI 50 123). Bulbar pouches were perfused with solutions of 0.9% Na C1, 0.1 N HC1, 40% glucose, 40% NaC1, and 40% peptone or with 0.1% solutions of acetylcholine chloride. Acidification of the bulbar pouches profoundly inhibited the acid output from the gastric ppoches. Perfusion with acetylcholine produced a transient inhibition of acid secretion. When hypertonic solutions were perfused through the bulbar pouches or the pouch of distal duodenum, no inhibition occurred. It is concluded that hypertonic solutions are not activators of the bulbar inhibitory mechanism that has been shown to respond to reduction of the intrabulbar pH. Inhibition following bulbar perfusion with acetylcholine may mean that liberation of the hypothetical humoral agent, bulbogastrone, to some extent is under cholinergic control.