Effect of acid secretory capacity and chronic endogenous hypergastrinemia on pancreatic secretion and intestinal morphology in the rat.

To study the trophic effects of gastrin on the gastrointestinal tract, chronic endogenous hypergastrinemia was produced in rats by implantation of the gastric antrum into the colon. Rats were sham-operated (normal gastrin, normal acid) or were prepared with BII gastrojejunostomy and antral resection (low gastrin, low acid), or BII gastrojejunostomy and antral implantation into colon (high gastrin, acid present). To separate effects of hypergastrinemia from those of acid hypersecretion, two additional groups were prepared with total gastrectomy and either resection of the antrum (low gastrin, no acid) or antral implantation into colon (high gastrin, no acid). After 12 weeks, the pancreatic secretory response to secretin was measured. The animals were then sacrificed, and liver, pancreas, small intestine, and colon were weighed. In separate groups of animals villous height and width and crypt depth of small intestine and transverse colon were measured. Serum gastrin concentrations increased three- to fivefold in fasting and fed antral implant animals. Serum gastrin levels in the fed state were lower in antrectomy rats compared to controls but did not differ in the fasting rats. Pancreas and colon were heavier in all hypergastrinemic rats. Liver weights did not differ between hypergastrinemic animals and controls. Stimulated pancreatic bicarbonate secretion following secretin infusion was elevated only in hypergastrinemic, hyperacidic rats. Hypertrophy of the small bowel was seen in antral implant rats only when the gastric remnant was preserved (ie, when acid was present). Colonic mucosal thickness was increased in antral implant rats with or without gastrectomy. No significant increases in small-bowel villous height or crypt depth were found in antral implant rats. Thus, chronic endogenous hypergastrinemia caused pancreatic and colonic hypertrophy independent of acid secretion. In addition to hypergastrinemia, gastric hyperacidity was also needed for enlargement of small bowel or increase in secretin-stimulated pancreatic bicarbonate secretion.