Experimental Studies on the Pathogenesis of Reflux Esophagitis

The roles of pepsin and sodium taurocholate in the production of acid reflux esophagitis were studied using the continuously perfused canine esophagus model. The hydrogen ion permeability as an index of mucosal barrier, elutions of carbohydrates and protein into the perfusate from the esophageal mucosa, and histochemical findings of injured mucosa were assessed. Sodium taurocholate caused severe disruption of the esophageal mucosal barrier. Pepsin eluted carbohydrates into the perfusate significantly. Histochemically, pepsin mainly eroded the superficial epithelium of the esophagus. In contrast, sodium taurocholate caused severe destruction of the esophageal glands in the deep layer. These results suggest a difference in the mechanism or site of injuries resulting from pepsin and sodium taurocholate. Furthermore, it was confirmed that sodium taurocholate inhibited the activity of pepsin to hemoglobin in an acid milieu.