Abstract

truncal vagotomized dogs. The concentration of serum 5-Hydroxytryptamine (5-HT) were measured before and after intragastric administration of MSG.MSG solution was administered into the stomach before feeding and gastric emptying was evaluated. Several antagonists were injected intravenously before MSG administration to the stomach. The effect of MSG was investigated in Pavlov (which was a vagally innervated corpus pouch), Heidenhain (which was a vagally denervated corpus pouch), and antral pouch (vagally innervated) dogs. Results: Upper gut motility was significantly increased by intragastric MSG but not significantly stimulated by intraduodenal MSG. Intragastric MSG did not induce a specific pattern such as an increase or decrease of serum 5-HT. Intragastric MSG (45 mM/kg) stimulated postprandial motility and accelerated gastric emptying. Moreover, intragastric and intraduodenum MSG at a dose of 90 mM/kg mostly induced retrograde migrating contractions in the jejunum, which propagated to the gastric body and were followed by vomiting. The MSG-induced contractions were inhibited by truncal vagotomy, atropine, hexamethonium, granisetron, and dopamine. The gut motility was increased by intrapouch injection of MSG in Pavlov pouch, but it was not affected in Heidenhain or antral pouch. Conclusions: Intragastric MSG stimulates upper gut motility and accelerates gastric emptying. The sensory structure of MSG is present in the gastric corpus, and the signal is mediated by the vagus nerve.

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