Pancreatic surgery, gastric secretion and ulcers in the rat. Increased ulcer development following pancreatic half resection or duct occlusion.

In the rat, both partial resection of the pancreas and occlusion of the side branches of the biliodigestive duct were investigated with respect to their influence on gastric secretion (acid, pepsin, sodium), gastric mucosal blood flow (MBF), development of gastric ulcers, and gastrin and somatostatin in the blood. On the 14th postoperative day the exocrine pancreatic function is reduced and ulcer index and severity are significantly enhanced. There are no simultaneous changes in gastric secretion or MBF. Aortal gastrin was decreased and somatostatin was unchanged. We conclude that: in the rat, reduction of exocrine pancreatic function should be considered an ulcerogenic factor; factors others than gastric hypersecretion or reduced MBF are responsible for ulcer formation, and an etiological role of either circulating gastrin or somatostatin is doubtful.