The gastric mucosal barrier

Most gastroduodenal ulcer disease results from a weakness in the normal gas tric mucous barrier against the penetration of acid secreted by the stomach . Based on meticulous and insightful research, the distinguished physiologi st Franklin Hollander hypothesized that the stomach is protected against it s own acid secretion by a dynamic two-component mucus-mucosal barrier. Holl ander and his co-workers defined the physical and chemical characteristics of the mucus components of this barrier, as well as the defense provided by the surface epithelial cell layer, which he viewed as the second line of d efense (the second component). Barrier investigators at Mount Sinai demonst rated the effects of impairment of barrier function with resultant increase d back-diffusion of acid, and they defined the consequences of this acid pe netration into the gastric epithelium. The contribution of these workers in cluded important observations on the natural impermeability of the gastric corpus and fundus as well as the normally increased permeability of the ant rum. They also presented evidence on the role of bile in duodenogastric ref lux in gastric ulcer disease and the presence of impaired barrier function in patients with gastric ulcer and pernicious anemia. Further studies inclu ded demonstration that stress and carcinogens could disrupt the gastric muc osal barrier. Disruption of the barrier, in turn, was shown to allow carcin ogenesis to occur by permitting the absorption of certain carcinogens which otherwise are warded off by the barrier. The Hollander two-component gastr ic mucosal barrier hypothesis has, in recent years, been increasingly valid ated by experimental data coming from other laboratories.