EPITHELIAL-CELL HYPERPROLIFERATION AFTER BILIOPANCREATIC REFLUX INTO THE ESOPHAGUS OF RATS

Background. Chronic reflux of duodenal contents into the esophagus of rats produces severe esophagitis and exerts a co-carcinogenic effect o n the proliferating cells by enhancing the formation of nitrosamine-in duced esophageal carcinomas. We investigated the effect of the differe nt components of the duodenal reflux on the epithelial cell proliferat ion of the lower esophagus. Methods. Sprague-Dawley rats underwent thr ee surgical reflux models (biliopancreatic, pancreatic, and biliary) a nd a sham operation. Animals were sacrificed at 72 hours, 6 weeks, and 9 weeks after the operation. Histology and cell proliferation, determ ined by ornithine decarboxylase activity, polyamine (putrescine, sperm idine, spermine) levels, and proliferating cell nuclear antigen labeli ng index of the basal and suprabasal layers, were studied in the dista l esophagus. Results. Both biliopancreatic and pancreatic reflux induc ed severe esophagitis starting on week 6. Suprabasal proliferating cel l nuclear antigen labeling index significantly increased throughout th e 9 weeks of the study in the biliopancreatic and pancreatic reflux gr oups, although this increase was earlier in the former group. Omithine decarboxylase activity and polyamine levels were significantly increa sed in the biliopancreatic and pancreatic groups on week 6, decreasing on week 9. Conclusions. Increased esophageal cell proliferation after both biliopancreatic and pancreatic reflux into the lower esophagus m ay therefore be one mechanism by which duodenal-content reflux stimula tes esophageal carcinogenesis in experimental animals. (C) 1998 by The Society of Thoracic Surgeons.