Abstract
The gastric mucosal barrier consisting of mucous and mucosal barriers in the rat is known to protect the gastric mucosa from the digestive activity of the gastric juice. The postulation by Plessis (1) that the permeability change of the gastric mucosal barrier is the main trigger in generating the gastric ulcer is originates from the observation that bile juice frequently present in the stomach of patients with gastric and duodenal ulcers induces the decreased secretion of the gastric mucus, by which the gastric mucosa is made more sensitive to the gastric acid there by activating the development of ulcers. Intragastric administration of bile juice in the dog was reported by Davenport (2) to result in the destruction of the mucosal barrier and the back diffusion of hydrogen ion to the mucosal layer. Similar results were recently obtained by the same procedure in humans (3). Decreased response of the gastric acid secretion to alcohol, caffein, or histamine in patients with gastric ulcers was also due to the back diffusion of hydrogen ion caused by the destruction of the gastric mucosal barrier (4, 5).
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