Hypergastric acid secretion in rats with ventromedial hypothalamic lesions

Abstract

This study was designed to investigate abnormal gastric acid secretion in ventromedial hypothalamic (VMH)-lesioned rats. Basal secretion and secretion stimulated by pentagastrin (25 μg/kg, IP) or histamine (2 mg/kg/h, IV) were significantly higher in VMH-lesioned rats than in sham VMH-lesioned rats. Subdiaphragmatic vagotomy and methyl atropine treatment (5 mg/kg, IV) remarkably decreased both basal (about 36–44%) and stimulated secretion (about 36–67%) in VMH-lesioned rats, but did not completely reverse it to normal. Serum insulin and glucose levels were significantly higher in VMH-lesioned rats, but serum gastrin levels were not. VMH-lesioned rats showed significantly heavier gastric dry weight; however, no difference in the mucosal layer/total layer ratio of the gastric wall and the density of the parietal cells was observed between the two groups, indicating that the total number of parietal cells might have increased in VMH-lesioned rats because the increase of gastric dry weight can be presumed to be due to increase of the gastric mucosal layer as well as total layer. These results suggest that vagal activation is one of the main contributors to hypergastric acid secretion in VMH-lesioned rats, but that other factors such as increase of parietal oxyntic cell number may also contribute.