OBJECTIVE: To understand the role of nitric oxide in the protection mechanism for the gastric mucosa in rats provided by omeprazole. METHODS: Intravenous injections with omeprazole, N -nitro-L-arginine methyl ester (L-NAME), L-arginine, or D-arginine were administered in rats with gastric mucosal lesion induced by pure ethanol. Gastric mucosal blood flow (GMBF), pH of the gastric juice and gastric mucosal NO 2 /NO 3 ratio were determined and the changes of ulcer index and the severity of tissue necrosis and neutrophil infiltration observed. RESULTS: The ulcer index of rats with omeprazole treatment was much lower than that of the control group (P<0.01) with lesser degree of tissue necrosis and neutrophil infiltration (P<0.01). The protective effect of omeprazole was significantly inhibited by prior administration of L-NAME that, however, was antagonized by prior administration of L-arginine, but not D-arginine. Intravenous omeprazole administration obviously increased GMBF and gastric mucosal NO-2 /NO 3 ratio, and such effect, apart from its action against secretion, could be counteracted by pretreatment with L-NAME. CONCLUSION: Omeprazole can exert important protection against gastric mucosal lesion in rats mediated by nitric oxide, and the action of omeprazole against gastric acid secretion contributes little to the protective effect.
OBJECTIVE: To understand the role of nitric oxide in the protection mechanism for the gastric mucosa in rats provided by omeprazole. METHODS: Intravenous injections with omeprazole, N -nitro-L-arginine methyl ester (L-NAME), L-arginine, or D-arginine were administered in rats with gastric mucosal lesion induced by pure ethanol. Gastric mucosal blood flow (GMBF), pH of the gastric juice and gastric mucosal NO 2 /NO 3 ratio were determined and the changes of ulcer index and the severity of tissue necrosis and neutrophil infiltration observed. RESULTS: The ulcer index of rats with omeprazole treatment was much lower than that of the control group (P<0.01) with lesser degree of tissue necrosis and neutrophil infiltration (P<0.01). The protective effect of omeprazole was significantly inhibited by prior administration of L-NAME that, however, was antagonized by prior administration of L-arginine, but not D-arginine. Intravenous omeprazole administration obviously increased GMBF and gastric mucosal NO-2 /NO 3 ratio, and such effect, apart from its action against secretion, could be counteracted by pretreatment with L-NAME. CONCLUSION:Omeprazole can exert important protection against gastric mucosal lesion in rats mediated by nitric oxide, and the action of omeprazole against gastric acid secretion contributes little to the protective effect.