Gastric mucosal defense after superficial injury.

Breaking of the "gastric mucosal barrier" has classically been perceived as an event with deleterious consequences. The implications have been that these disruptions may lead to gastric ulceration. Contrary to this view, recent experimental evidence has shown that the superficial epithelium is not only focally disrupted during alcohol, drug, and food ingestion, but, under non-pathological conditions, the epithelial barrier is rapidly repaired in about one hour or less by migrating mucous cells. After an initial insult to the superficial mucosa, which does not produce a hemorrhagic lesion, the interfoveolar necrotic epithelium exfoliates slightly into the gastric lumen covering the damaged mucosa. This layer of mucus and dead cells shields the mucosa from further damage by luminal necrotizing agents, in addition to trapping alkaline exudate from the capillaries next to the newly forming epithelium. Each of these responses to superficial injury--formation of a protective mucoid layer, flow of alkaline "mucosal fluid" to dilute luminal noxious agents, rapid epithelial restitution of the superficial cells--appears to prevent the formation of deeper hemorrhagic lesions. These data suggest that factors which facilitate or impede these 3 mucosal defense mechanisms may be of greater concern in the etiology of acute gastric erosions than the "integrity of the gastric mucosal barrier," as classically viewed.