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Ann Thorac Surg 1998;65:779-786
© 1998 The Society of Thoracic Surgeons

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Original Articles: General Thoracic

Epithelial Cell Hyperproliferation After Biliopancreatic Reflux Into the Esophagus of Rats

Department of Surgery, Hospital Clinic i Provincial, University of Barcelona Medical School, Barcelona, Spain
Department of Pathology, Hospital Clinic i Provincial, University of Barcelona Medical School, Barcelona, Spain,
Department of Plant Physiology, Faculty of Pharmacy, University of Barcelona, Barcelona, Spain

Dr Pera, Service of General Surgery, Hospital Clinic i Provincial, University of Barcelona Medical School, Villarroel 170, Barcelona 08036, Spain (e-mail: pera@medicina.ub.es).

Abstract presented at the Thirty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Feb 3–5, 1997.

Background. Chronic reflux of duodenal contents into the esophagus of rats produces severe esophagitis and exerts a co-carcinogenic effect on the proliferating cells by enhancing the formation of nitrosamine-induced esophageal carcinomas. We investigated the effect of the different components of the duodenal reflux on the epithelial cell proliferation of the lower esophagus.

Methods. Sprague-Dawley rats underwent three surgical reflux models (biliopancreatic, pancreatic, and biliary) and a sham operation. Animals were sacrificed at 72 hours, 6 weeks, and 9 weeks after the operation. Histology and cell proliferation, determined by ornithine decarboxylase activity, polyamine (putrescine, spermidine, spermine) levels, and proliferating cell nuclear antigen labeling index of the basal and suprabasal layers, were studied in the distal esophagus.

Results. Both biliopancreatic and pancreatic reflux induced severe esophagitis starting on week 6. Suprabasal proliferating cell nuclear antigen labeling index significantly increased throughout the 9 weeks of the study in the biliopancreatic and pancreatic reflux groups, although this increase was earlier in the former group. Ornithine decarboxylase activity and polyamine levels were significantly increased 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 may therefore be one mechanism by which duodenal-content reflux stimulates esophageal carcinogenesis in experimental animals.

This article has been cited by other articles:

				M. Pera, P. L Fernandez, M. Pera, A. Palacin, A. Cardesa, C. Dasenbrock, T. Tillman, and U. Mohr Expression of cyclin D1 and p53 and its correlation with proliferative activity in the spectrum of esophageal carcinomas induced after duodenal content reflux and 2,6-dimethylnitrosomorpholine administration in rats Carcinogenesis, February 1, 2001; 22(2): 271 - 277. [Abstract] [Full Text] [PDF]

				M. Pera, M. J. Brito, M. Pera, R. Poulsom, E. Riera, L. Grande, A. Hanby, and N. A. Wright Duodenal-content reflux esophagitis induces the development of glandular metaplasia and adenosquamous carcinoma in rats Carcinogenesis, August 1, 2000; 21(8): 1587 - 1591. [Abstract] [Full Text] [PDF]