Abstract
Acute stimulation of gastric acid secretion as well as intragastric instillation of physiological concentrations and volumes of HCl caused marked changes in the appearance of surface epithelial cells of the stomach. These changes could represent a damage of the gastric surface epithelial cells of the stomach. Pretreatment with the histamine H2-receptor-blocking drug cimetidine tended to reduce this damage, although the difference was not significant. In contrast, it was completely abolished by an analogue of prostaglandin E2. These observations suggest that gastric epithelial cells may be damaged under physiological conditions and that quick repair is needed to prevent ulceration of the gastric mucosa. Alternatively, endogenous release of prostaglandin under certain undefined conditions could prevent this damage.

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