Abstract-We examined the role of gastric ammonia in the development of gastric lesions in rats. Exposure of the gastric mucosa to ammonia (30 mM) produced microscopic injury, but no macroscopic lesion was observed.However, exposure of the stomach to ammonia in rats subjected to ischemia resulted in macroscopic gastric lesions.The macroscopic lesions were markedly inhibited by pretreatment with taurine, a scavenger of hypochlorous acid (HOCI) and monochloramine (NH2CI). These results indicate that ammonia is deleterious to gastric mucosa, and monochloramine may be involved in the pathogenesis of ammonia-induced mucosal lesions.Recent evidence suggests that reactive oxygen metabolites (02-, H202) are mediators of the tissue injury associated with ischemia

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Abstract-We examined the pathophysiological roles of the urea-urease-ammonia system in gastric ulcer disease using rats. Exposure of the stomach to ammonia (0.01-1.0%) decreased the transmucosal potential difference (PD) and histological injury in a concentration-dependent manner.Exposure of the stomach for 20 min to urea (0.025-0.2%) together with urease (100 IU) produced a decrease in PD and microscopic injury similarly, and the lesion was closely associated with the amount of ammonia produced.Urea and urease alone had no effect on the gastric mucosa.These results suggested the pathophysiological importance of urea, urease and ammonia in gastric ulcer disease.

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