Gastric motility responses to duodenal stimulation of an in vitro rabbit stomach-duodenum preparation

Abstract

Regulated gastric emptying is necessary for the complete digestion and absorption of intestinal chyme. However, experiments have shown that the extrinsic denervation of stomach and duodenum does not result in a cessation of gastric function. Furthermore, the components necessary for the integration and relay of neural information have been demonstrated in the intrinsic nervous network of the gut. A possible hypothesis therefore, is that the enteric nervous system may playa role in the regulation of gastric function. The purpose of this study was to establish whether or not stimulation of the duodenal mucosa of an in vitro rabbit stomach-duodenum preparation has any effect on gastric motility. Electrically stimulated changes in intragastric pressure were used as indicators of gastric motility and recorded with an intragastric balloon connected to a transducer and chart recorder. The records were made in both the presence and absence of mechanical and chemical stimulation of the duodenal mucosa. A comparative analysis was carried out on the frequency and amplitude of electrically stimulated gastric contractions, and of the peristaltic contractions that took place after electrical stimulation of the stomach wall. The results were found to differ depending on the type of duodenal stimulus applied. Duodenal distension did not attenuate or amplify the subsequent gastric response to electric stimulation of the stomach wall. However, a disturbance in the inherent pattern of gastric peristaltic contractions was observed. In contrast, the presence of hydrochloric acid in the duodenum, reduced the force of the electrically stimulated gastric contraction by half, but the inherent pattern of peristalsis that followed the electrical stimulation appeared unaltered. These results suggest the existence of a gastric motility regulation mechanism in the rabbit that is mediated by the enteric nervous system and that responds to stimulation of the duodenal mucosa.