Antral proliferation of G cells after truncal, parietal cell, and antral vagotomy

Abstract

Antral gastrin cell numbers and serum gastrin levels were studied in five groups of rats: (1) control, (2) truncal vagotomy, (3) truncal vagotomy with pyloroplasty, (4) parietal cell vagotomy, and (5) antral vagotomy. Female Sprague-Dawley rats weighing approximately 225 g were used. Eighteen days after operation radiographic study was performed to assess gastric size and emptying rate. At sacrifice serum was obtained for gastrin assay, gastric pH measured, and the antrum removed for G-cell quantitation. Gastric pH was elevated in all groups except antral vagotomy. Variable degrees of gastric distention and delayed gastric emptying were observed in the rats with truncal vagotomy alone, truncal vagotomy plus pyloroplasty, and antral vagotomy. Parietal cell vagotomy rats had no change in gastric size or emptying rate. Rats with truncal vagotomy, truncal vagotomy plus pyloroplasty, and parietal cell vagotomy had significant increases in serum gastrin levels and in G-cell density. Antral vagotomy resulted in no significant differences from controls. A gastrin inhibitory mechanism residing in the corpus may become inoperative after vagal denervation. Alternatively, proliferation of G cells and increased serum gastrin levels may be a consequence of decreased luminal acid after vagotomy. Vagal innervation of the corpus is a critical variable in control of the antral G-cell mass, but antral innervation is not. Distention by itself does not seem to produce G-cell hyperplasia.