Role of local secretory and motility changes in the pathogenesis of experimental duodenal ulcer.

Changes in gastric acid and pepsin secretions do not fully account for the duodenal ulcerogenic effect of cysteamine or propionitrile in the rat. We investigated the role of pancreatic and biliary secretions as well as motility changes in the duodenum. Bypass of bile to the jejunum and/or ablation of pancreatic secretion or drainage of these secretions through chronic duodenal fistula aggravated the cysteamine-induced duodenal ulcers. Biliary bypass to the proximal duodenum, on the other hand, decreased the incidence and intensity of experimental duodenal ulcers. An increased and dopamine-sensitive myoelectric activity caused by cysteamine or propionitrile was recorded in the proximal duodenum, indicating a state of hypermotility. Indeed, a decreased quantity of bilirubin was recovered through the chronic fistula in the proximal duodenum, suggesting an impaired delivery of bile to the ulcer area after cysteamine administration. Thus, duodenal hypermotility probably prevents the proper mix and neutralization of gastric acid and duodenal (mucosal, biliary and pancreatic) secretions, predisposing to ulceration in the proximal duodenum.