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Exogenous prostaglandin(PG) E2, 5 pglkg, was orally administered to DONRYU rats. Then, the animals were immersed in water to induce gastric ulcers. Postmortal macroscopic examinations of the stomach revealed that exogenous PGE2 markedly prevented the occurrence of ulcers. In contrast to the control (immersed in water without PGE2 pretreatment), the experimental group showed (1) a slight increase in endogenous PGE at Stages II and III, (2) a marked decrease in glandular kallikrein (GK) at all stages and (3) no change in tissue plasminogen activator (TPA) at any stage. On the other hand, endogenous PGE in the group untreated with PGE2 showed a marked increase at Stage I and a moderate decrease at Stages II and III compared with findings obtained from the corresponding control (neither treated with PGE2 nor immersed in water). Our previous studies demonstrated that GK gradually decreased with the progress of stage, and that TPA markedly increased at Stage I and gradually decreased at Stages II and III. These findings suggest that PGE may interact

Relation between tissue prostaglandins and the kinin-fibrinolysis system during the course of experimental gastric ulcers formation in rats