Meal-stimulated exocrine pancreatic secretion and release of GI peptides in normal and nicotine-treated rats.

In rats, treated chronically with saline and nicotine, we studied the postprandial release of gastrin and cholecystokinin by specific radioimmunoassays and simultaneously measured secretory outputs of the exocrine pancreas. Rats were prepared surgically with gastric and pancreatic fistulas. Meal-stimulated release of peptides and exocrine secretory outputs were measured 24 h postoperatively in conscious rats. Infusion of food via intragastric cannula significantly stimulated plasma gastrin levels in both control and nicotine treated rats. Postprandial gastrin levels in nicotine treated rats were significantly higher compared to gastrin levels obtained after food in untreated control rats. Plasma CCK levels were increased in both groups after food. These levels remained significantly elevated from the basal values only for a transient period following infusion of the liquid meal. There were no differences in postprandial plasma CCK levels between the two groups. Outputs of exocrine pancreatic volume, protein and trypsin increased significantly after food in both control and nicotine treated groups of rats. The differences in outputs of volume and protein between the two groups of rats were not significant; however, the trypsin outputs in the nicotine rats were decreased significantly when compared to control rats. The data indicate that in rats, administration of food stimulated the release of immunoreactive gastrin and CCK with concomitant increase in exocrine pancreatic secretions of volume, protein and trypsin. Chronic nicotine treatment and its effect on food, however, appeared to have induced hyperfunction of G-cells that resulted in increased gastrin secretion and a decrease in trypsin secretion by exocrine pancreas. These data may have important implications in the etiology of the development of exocrine pancreatic dysfunction in chronic smokers.