Contribution of gastrin to cysteamine-induced gastric acid secretion in rats.

The role of circulating gastrin in cysteamine induced gastric acid secretion was examined in conscious male Wistar rats, provided with a portal vein catheter, a jugular vein catheter and a pyloric drainage tube. Intravenous infusion of 0.3 nmol/kg.30 min of gastrin 17-l resulted in serum gastrin concentrations of 1138 +/- 151 pg/ml and gastric acid secretion of 104 +/- 36 mumol H+/kg.30 min. This acid response was abolished by intravenous injection of 60 microliters of a gastrin-antiserum, indicating the efficacy of immunoneutralization with this antiserum in vivo. Intravenous bolus administration of 125 mg/kg of cysteamine induced increases in serum gastrin concentration (864 +/- 96 pg/ml) and gastric acid outputs (107 +/- 27 mumol H+/kg.30 min) not significantly different from the gastrin 17-l infusion experiments. Gastrin antiserum abolished cysteamine-induced gastric acid secretion, indicating that gastric acid secretion induced by 125 mg/kg of cysteamine is largely mediated by circulating gastrin in rats.

Inhibition of meal-stimulated gastric acid secretion by gastrin immunoneutralization in rats.

Gastrin 17-I was infused into conscious rats equipped with jugular and portal vein catheters and with a pyloric gastric drainage tube to achieve serum concentrations slightly higher than those found during intragastrically instilled peptone solutions. I.v. injected rabbit gastrin antiserum abolished gastrin 17-I-stimulated gastric acid secretion in these animals. Gastrin immunoneutralization reduced peptone-stimulated gastric acid secretion by approximately 37% during the entire 30-min period of stimulation. Peptone-stimulated gastric acid secretion was only significantly (P less than 0.05) inhibited in the third 10-min period, but not in the first or second 10-min periods of stimulation. This study demonstrates that the late but not the initial period of peptone-stimulated gastric acid secretion is regulated by circulating gastrin in rats.

Effects of lorglumide on gastrin- and peptone-stimulated gastric acid secretion in rats.

This study in rats demonstrates that gastric acid secretion stimulated by infusion of gastrin 17-I yielding plasma concentrations in the physiological range is almost abolished by the cholecystokinin-receptor antagonist lorglumide. Furthermore, lorglumide also inhibited intragastric peptone stimulated gastric acid secretion by 43%. When compared to peptone stimulation with a saline background infusion, lorglumide infusion inhibited peptone stimulated gastric acid secretion only significantly in the late (20 to 30 minutes) part of stimulation, while the initial part (0 to 10 and 10 to 20 minutes) was not significantly inhibited by lorglumide. Both peptone stimulation and gastrin infusion significantly augmented serum gastrin concentrations, which were not significantly influenced by lorglumide. The serum gastrin concentrations achieved during gastrin infusion were higher than during peptone stimulation, however the differences were not statistically significant. It is concluded that lorglumide abolishes gastrin stimulated gastric acid secretion in rats, but only partly (43%) inhibits peptone-meal stimulated gastric acid secretion. In contrast to the gastrin infusion experiments, where lorglumide abolishes acid secretion during the entire study period, the compound inhibits gastric acid secretion more effectively towards the end of peptone stimulation than in the beginning.