Bile acids are one of the noxious components of the gastroduodenal contents which may injure the esophageal mucosa in clinical reflux esophagitis. Animal models of esophagitis have shown that exposure to low luminal bile acid concentrations can cause increased mucosal permeability to a variety of ions and molecules without causing dramatic gross morphologic damage. In order to explore the mechanism by which bile acids alter mucosal permeability, we measured the esophageal mucosal concentration of taurocholic acid and chenodeoxycholic acid after exposure to these bile acids in anesthetized New Zealand white rabbits. We found that bile acids can accumulate in the esophageal mucosa to levels as high as seven times the initial luminal concentration. Thin-layer chromatography showed that this accumulation was not due to bile acid degradation in the mucosa. Since butyric acid also showed some mucosal accumulation, and is a weak acid like taurocholic acid, intracellular ionization may account for some of the accumulation. Mucosal accumulation of these molecules is not a nonspecific phenomenon, since the four-carbon polyol erythritol did not accumulate at all. Bile acid accumulation occurred under the same conditions and in a parallel temporal relationship to the bile-induced permeability changes. It is hypothesized, therefore, that the presence of high concentrations of bile acids in the esophageal mucosa may be pathophysiologically related to the alterations in mucosal permeability which occur after exposure to bile acids.
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