Abstract
LUMINAL acid is generally accepted as essential for the pathogenesis of gastric ulceration. Although the role of acid has been widely investigated, other factors that affect gastric-mucosal resistance to injury have only begun to receive attention. Recent studies show that mucosal permeability and blood flow, secretory state, acid–base balance and the presence of pepsin influence the gastric-mucosal response to luminal acid, and that carbonic anhydrase and prostaglandins within the mucosa probably have an important role in protection against damage. This paper presents some concepts of the pathogenesis of experimental gastric-mucosal injury that have evolved during the past 10 years. Mucosal . . .
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