Prostaglandin generation in the gastric mucosa of rats with stress ulcer.

Prostaglandins, normally synthesized by the gastric mucosa, have been shown to prevent the formation of experimentally induced ulcers, including stress ulcers. A physiologic role of these compounds in the protection of the gastric mucosa has been postulated. In order to assess the role of endogenous prostaglandins in the pathogenesis of stress ulceration, we measured the amounts of prostaglandin E (PGE) generated by gastric mucosal samples from rats exposed to cold restraint stress. Stress induced a significant inhibition of PGE biosynthesis by the gastric mucosa. The inhibition was similar to that caused by indomethacin. The degree of inhibition of PGE generation significantly correlated with the severity of the gastric mucosal lesions (P less than 0.001). Identical effects were identified in antrum and fundus. The decrease of PGE mucosal biosynthesis seems to be a major determinant in the pathogenesis of stress ulceration.