抄録
A standard method for the production of gastric lesions by aspirin in rats was elaborated, and the mechanisms of the deleterious effects of aspirin were interpreted. The method consisted of pylorus ligation of the rat immediately before aspirin dosing, resulting in severe and consistent gastric lesions in the glandular portion of the rat stomach 7 hr later. Sodium bicarbonate and L-glutamine showed a strong inhibitory effect on the development of aspirin-induced lesions, at almost the same dose level. Aspirin itself reduced the gastric acidity in pylorus-ligated rats. Sodium bicarbonate with or without aspirin markedly lowered the gastric acidity, whereas L-glutamine with or without aspirin restored the reduced acidity by aspirin or increased the acidity more than the normal level. These findings suggest that Lglutamine may inhibit the back diffusion of HCl into the gastric mucosa caused by aspirin. Amylopectine sulfate and sulfated glyptide, in a dose sufficient to suppress the peptic activity of gastric contents, slightly inhibited the aspirin-induced lesions. Atropine sulfate, which strongly reduced gastric juice volume but not acidity, did not exert a marked influence on aspirin-induced lesions.
