Studies on the release of extra‐antral gastrin evidence of vagal inhibition in the dog

Abstract

AbstractSerum gastrin concentration was measured in 3 dogs after a meat meal; basal levels rose significantly after 10 minutes. After antrectomy with a Billroth I, and later a Billroth II anastomosis, the tests were repeated. Basal gastrin levels were unchanged but the rise after meat feeding was abolished. Four antrectomized dogs with a BII anastomosis and cannulae in both the duodenum and stomach were used to examine the effect of duodenal perfusion on serum gastrin. Whether the perfusate was 150 mM NaCl, 150 mM HCl or 0.1% acetylcholine, the mean serum gastrin levels did not differ significantly from basal levels. Transthoracic vagotomy in antrectomized dogs produced a significant rise in basal gastrin levels, but did not restore the response to a meat meal or duodenal perfusion.Parallel studies were conducted in 6 antrectomized, vagotomized patients who had undergone Roux‐en‐Y conversion for postgastrectomy bilious vomiting, and in 2 patients after total gastrectomy. Duodenal perfusion via duodenostomy tubes with 150 mM NaCl, 150 mM HCl, fat emulsion, and an amino acid mixture did not raise serum gastrin above basal levels.Since meat feeding and duodenal perfusion in antrectomized dogs and humans failed to stimulate a rise in serum gastrin, we conclude that the intestinal phase of gastric secretion is unlikely to be mediated by gastrin. The results following vagotomy in the dog suggest that extragastric basal gastrin release is vagally inhibited or that vagotomy interferes with the catabolic destruction of gastrin.