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[Gastric lesions induced by ethanol and indomethacin: cytoprotective effect of acetazolamide]
1Universidad Nacional de Rosario, Argentina.
Abstract:
A study was made of the effect of acetazolamide (a potent carbonic anhydrase inhibitor) on the production of lesions by absolute alcohol and of the effect of indomethacin (inhibitor of cyclooxygenase) on the gastric cytoprotection produced by S-adenosylmethionine (sulfhydryl compound). Acetazolamide significantly reduced gastric mucosa lesions induced by oral administration of absolute alcohol. It did not modify those produced by indomethacin. Pretreatment with acetazolamide potentiated the production of S-adenosylmethionine in response to alcohol injury, but it did not modify the protective effect of S-adenosylmethionine against injury by indomethacin. Since acetazolamide did not alter gastric secretion of HCO3-, it is concluded that carbonic anhydrase-dependent gastric alkali secretion did not intervene in the gastric acetazolamide-induced cytoprotective mechanism. The same effect was produced by stimulation of the biosynthesis of endogenous prostaglandins. This provides a physiologic rationale for the use of acetazolamide in acute gastric disease and gastroduodenal peptic ulcer.
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