Role of histamine H2-receptors in gastric and pancreatic release of somatostatin-like immunoreactivity during the gastric phase of meal.

The present study was designed to determine the role of H2-receptors in the postprandial release of somatostatin-like immunoreactivity (SLI) from the gastric fundus and antrum and from the pancreas. In dogs subjected to laparotomy, the pylorus was bisected and a gastric fistula was created, following which 250 ml 20% liver extract (LE) at pH 7 or 2 were instilled intragastrically. In the fundic vein the incremental SLI rise in response to LE at pH 7 was 2423 plus or minus 540 pg/ml during a control infusion of saline and 4780 plus or minus 863 pg/ml during the infusion of cimetidine (1 mg/kg per h) (P less than 0.05). In the antral vein the incremental SLI in response to LE at pH 7 was 2182 plus or minus 530 pg/ml during the saline control but did not rise significantly during cimetidine infusion. In the pancreatic vein the incremental SLI level after LE at pH 7 was 1953 plus or minus 358 pg/ml in the control experiments and 4430 plus or minus 1024 pg/ml during cimetidine infusion (P less than 0.025). The incremental inferior vena cava SLI level was approximately 925 pg/ml in both groups (not significant). The instillation of LE at pH 2 during the saline control lowered fundic vein SLI by 500 pg/ml; this decline was abolished during cimetidine infusion. In the antral vein the incremental SLI level of 15 750 plus or minus 2514 pg/ml during saline was lowered to only 6728 plus or minus 2257 pg/ml during cimetidine (P less than 0.025). After LE at pH 2 the incremental pancreatic vein SLI level of 5641 plus or minus 1175 pg/ml during the control infusion was also significantly reduced to 2392 plus or minus 559 pg/ml by cimetidine (P less than 0.05). The incremental SLI in the inferior vena cava was reduced from 1270 plus or minus 280 pg/ml during saline to 680 plus or minus 190 pg/ml when cimetidine was infused (P less than 0.05). The present data suggest a histaminergic influence via stimulation of H2-receptors upon the regulation of gastric and pancreatic somatostatin release during the gastric phase of a meal.