The effect of chronic acidification of the canine duodenum on gastrin release from the antrum transplanted into the colon

Abstract

Exogenous infusion of acid into the canine duodenum inhibits acid secretion stimulated by endogenously released and exogenously administered gastrin. The importance of this mechanism in normal acid homeostasis and in the inhibition of chronic endogenous acid hypersecretion is not established. In this study the classic Dragstedt model antral colonic transplant (ACT) was used to produce endogenous hypergastrinemia and acid hypersecretion. The effects of the ACT when the duodenum was retained in continuity with the stomach (gastroduodenostomy) were compared with those obtained when the duodenum was no longer in continuity with the stomach (gastrojejunostomy). The duodenum markedly suppressed gastrin release (p = 0.003) and gastric acid secretion (p = 0.005) in each of the four dogs. The dogs remained free of ulcers for 8 months after gastroduodenostomy and ACT. However, after conversion to gastrojejunostomy, large, chronic peptic ulcers developed after a mean of 3.5 months. The inhibitory effect of the duodenum on gastric release and gastric acid secretion protected the dog against ulceration for an extended period. The duodenum may be the major site of inhibitory control of acid secretion and endogenous gastrin release in dogs.