Responses of the murine esophageal microcirculation to acute exposure to alkali, acid, or hypochlorite

Abstract

Background/Purpose Although ingestion of alkali-based and/or hypochlorite-based household cleaners as well as strong acids remains a major cause of esophageal wall injury, little is known about the mechanisms that underlie the injury response to these toxic agents. This study examined the roles of vascular dysfunction and inflammation to the esophageal injury response to different caustic substances in mice. Methods The esophageal responses to sodium hydroxide (10%, 5%, and 2.5%), potassium hydroxide (10%, 5%, and 2.5%), sodium hypochlorite (5.25%), and hydrochloric acid (10%, pH 2) were evaluated by intravital videomicroscopy and histopathology. Intravital microscopy was used to monitor changes in the diameter of arterioles and venules, the adhesion and movement of leukocytes in venules, and the time of cessation of arteriolar blood flow in mouse esophagus. The esophageal mucosa was exposed to caustic substances for 0 to 60 minutes before evaluation. Results The higher concentrations of sodium hydroxide and potassium hydroxide elicited rapid stasis in both arterioles and venules, which was accompanied by arteriolar constriction and thrombosis. An accumulation of adherent leukocytes in venules was not observed with any agent. Histopathological evaluation revealed marked cellular and interstitial edema in the mucosa with alkali, whereas hydrochloric acid and sodium hypochlorite decreased the thickness epithelial layer. Conclusion These findings suggest that ischemia and thrombosis are dominant processes, whereas inflammation is less important in the pathogenesis of acute corrosive injury to the esophageal mucosa.