The role of luminal pH in production of gastrin cell hyperplasia in the rat

Truncal vagotomy is associated with diminished gastric acid production, gastrin cell hyperplasia, and elevated serum gastrin levels. To study the role of reduced antral luminal acidity in the production of gastrin cell proliferation, gastrin cell densities were quantitated in preparations involving exposure of the antral mucosa to a nonacid lumen at different levels of the gastrointestinal tract. Female Sprague-Dawley rats were divided into the following experimental groups: intact controls, shams, antral diverticulum on the jejunum, antral diverticulum on the ileum, and antral diverticulum on the colon. At death, 2 weeks, 2 months, and 6 months after operation, luminal pH was at least 5.8 for each group of rats with antral diverticula. No significant changes in gastrin cell numbers were observed in rats with jejunal or ileal diverticula. For those animals with colonic diverticula, gastrin cell counts were increased 55% at 2 weeks (503 ± 23 cells per cm versus 320 ± 13 cells per cm for shams). At 2 months gastrin cell numbers had increased further (639 ± 54 cells per cm) in rats with antral diverticula on the colon. Gastrin cell proliferation was sustained at 6 months in this group. A factor other than reduced luminal acidity induces gastrin cell proliferation in antral mucosa exposed to colonic content. The responsible agent is not present in the small-bowel lumen. A nonacid luminal environment is not, by itself, a sufficient stimulus for gastrin cell hyperplasia.