Evidence for an Enterogastric Reflex for the Inhibition of Acid Secretion

Abstract

In order to identify the mechanisms responsible for the inhibition of gastric secretion observed during acidification of the duodenal bulb, dogs were prepared with a gastric fistula (GF), Heidenhain pouch (HP), and pancreatic fistula. The duodenal bulb (5 cm) was separated from the stomach by a mucosal septum at the pyloric end and was brought to the surface in a mucocutaneous fistula distally. After the first series of experiments were completed, the dogs were reoperated and the duodenal bulb was completely separated from the stomach. The experiments were then repeated. Perfusion of the innervated duodenal bulb with 8 mEq of HC1 per hr resulted in 50% inhibition of pentagastrin (2 μg per kg-hr) -induced acid secretion from the GF and slight stimulation of pancreatic volume, bicarbonate, and protein output. Acid and pepsin secretion from the HP were unchanged by acidification of the bulb. A small dose of synthetic secretin (0.2 U per kg-hr) increased pancreatic secretion more than did bulbar acidification but did not inhibit acid secretion. A larger dose of secretin (1.6 U per kg-hr) caused 50% inhibition of acid secretion from both the GF and HP. Following the surgical separation of the duodenal bulb from the pylorus, acidification of the bulb failed to inhibit gastric secretion from the GF as well as from the HP. We interpret these results as evidence for the existence of a neural reflex, triggered by acid in the duodenal bulb, and inhibiting gastric secretion. Earlier studies by several groups have shown that acidification of the bulb inhibited HP secretion, thus indicating a hormonal mechanism. We cannot explain the failure to find evidence of such a mechanism in this study.