Effect of gastric vagal denervation on inhibition of acid secretion by secretin.

Abstract

In dogs with vagally innervated gastric pouches and gastric fistulas, acid secretion was stimulated by intravenous administration of Urecholine, 0.025 and 0.1 (mg/kg)/hr; of pentagastrin, 4 (µg/kg)/hr; or by feeding a meal of liver and bone dust, 25 g/kg. Acid secretion elicited by these stimulants was significantly inhibited (P<0.05 to 0.001) by intravenous infusion of secretin, 2 (units/kg)/hr. With Urecholine, 0.1 (mg/kg)/hr, comparable inhibition resulted from endogenous duodenal acidification which was produced by closing the gastric fistula. The pouches were then vagally denervated by cutting the muscular connection, and dividing the septum between pouch and main stomach; all tests were repeated. Vagal denervation decreased the stimulatory potency of feeding and pentagastrin, but increased Urecholine-stimulated acid output. This increased sensitivity of parietal cells to a cholinomimetic stimulus after vagal denervation is an example of Cannon's law of denervation supersensitivity. Inhibition of Urecholine-stimulated secretion by duodenal acidification was not significantly modified by vagal denervation (40% inhibition before, 38% after). Percentage inhibition of acid output by secretin was slightly increased after vagal denervation when the stimulant was Urecholine (42% inhibition before, 52% after) or pentagastrin (63% inhibition before, 73% after), but these changes were not statistically significant. Vagal denervation markedly increased the degree of inhibition of food-stimulated secretion (20% inhibition before, 71% after), suggesting that secretin is primarily an antagonist of gastrin.