Gastric and Pancreatic Release of Somatostatin-like Immunoreactivity During the Gastric Phase of a Meal: Effects of Truncal Vagotomy and Atropine in the Anesthetized Dog

Abstract

The postprandial release of gastric and pancreatic somatostatin-like immunoreactivity (SLI) was examined in anesthetized dogs during the gastric phase of a meal, and the role of vagal and atropine-sensitive mechanisms in the responses was assessed. The intragastric instillation of liver extract at pH 7 elicited a significant rise in antral vein SLI (∼300 pg/ml) and gastrin concentration. After truncal vagotomy, both baseline and postprandial antral vein SLI and gastrin concentration increased significantly compared with the control group. The infusion of atropine (100 μg/kg/h) abolished the postprandial rise in antral vein SLI but not in gastrin. The liver meal at pH 2 elicited a sustained sixfold greater rise of antral SLI (∼2000 pg/ml) than that at pH 7, while gastrin concentrations did not rise significantly. The latter antral SLI response was not influenced by truncal vagotomy, but atropine infusion reduced it by about 50%. In response to the meal at pH 7, fundic vein SLI concentrations rose by about 300 pg/ml. The rise was augmented slightly by truncal vagotomy but was abolished completely by atropine infusion. In response to the meal at pH 2, fundic SLI decreased sharply below baseline levels. The response was not altered significantly by vagotomy, but was reversed completely by atropine infusion, during which fundic vein SLI concentrations rose significantly. Pancreatic vein SLI concentrations rose by about 350 pg/ml in response to the gastric meal at pH 7. That rise was not altered significantly by vagotomy but was abolished by atropine infusion. In response to the meal at pH 2, pancreatic SLI concentrations rose by about 1000 pg/ml above baseline, significantly greater than the response to the meal at pH 7. The pancreatic vein SLI response to the meal at pH 2 was not altered by vagotomy. It was reduced considerably by atropine infusion. It is concluded that SLI is released from the antrum, fundus, and pancreas during the gastric phase of a meal and that these responses are modified by acidification of the intragastric contents and by truncal vagotomy and atropine infusion. The greatly augmented release of antral SLI in response to the acidified meal raises the possibility of a role for somatostatin in acid-induced suppression of gastrin release.