Bile Reflux Esophagitis

Abstract

This study was designed to determine the relative contribution of acid and/or duodenal contents on development of reflux esophagitis in the rat. Gross and microscopic changes in the esophageal mucosa at 10, 15, 30, and 60 days were recorded in sham-operated animals and in two experimental groups. One study group had a transsection of the esopha-gogastric junction (model I), and the other a total gastrectomy (model II). Bowel continuity was reestablished by esophagojejunal anastomosis. Subgroups of both animal models received either no treatment or cholestyramine or aluminum phosphate for 30 days in drinking water. At 30 days a similar degree of esophagitis was found in the untreated animals of both study models. Cholestyramine improved the degree of esophagitis in model II, whereas aluminum phosphate increased mucosal alterations in model I. At 60 days, 50% of the animals no longer had esophagitis and had regained satisfactory nutritional status. It is concluded that: (1) bile reflux is a major factor in esophagitis; (2) cholestyramine protects against bile reflux, and (3) proper nutritional status is of major importance in mucosal healing.

The role of alkaline reflux in esophageal carcinogenesis induced by N‐amyl‐N‐methylnitrosamine in rats

“…Since Helsingen's experiments (1959;1960), many experiments attempting to elucidate the pathogenesis of reflux esophagitis have been performed (Henderson et al, 1972;Siroos et al, 197.5;Salmon and Hem, 1981;Mud et al, 1982;Lehnert et al, 1983). Levrat et al (1962) concluded that reflux esophagitis develops when duodenal contents regurgitate into the esophagus.…”