Aim: Acetylsalicylic acid (ASA, aspirin), which is one of the most frequently used drugs in the world, causes severe gastric mucosal injury. Nitric oxide (NO) is synthesized from L-arginine by nitric oxide synthase (NOS). NOS can be inhibited by Nω-nitro-L-arginine methyl ester (L-NAME) and stimulated by supplementing the diet with L-arginine (L-Arg). The aim of this study was to investigate the role of NO on gastric mucosal injury induced by ASA. Materials and Methods: Male Sprague-Dawley rats were divided into seven groups: control, ASA, ASA+L-NAME, ASA+L-Arg, ASA+L-Arg+L-NAME, only L-NAME, and only L-Arg groups. After administration of the drugs, the rats were decapitated and their stomachs were removed and fixed in 10% neutral-buffered formalin solution. Results: Mucosal erosion, intramucosal hemorrhage, inflammatory cell infiltration, gland cell detachment, and necrosis were observed in the ASA group. It was demonstrated that L-Arg administration decreased the gastric mucosal injury, whereas L-NAME administration increased the extent and severity of the gastric injury induced by ASA. L-Arg or L-NAME administration alone did not affect gastric mucosa. Conclusions: We concluded that NO may have protective effects on gastric mucosal injury induced by ASA.

Aim: Acetylsalicylic acid (ASA, aspirin), which is one of the most frequently used drugs in the world, causes severe gastric mucosal injury. Nitric oxide (NO) is synthesized from L-arginine by nitric oxide synthase (NOS). NOS can be inhibited by Nω-nitro-L-arginine methyl ester (L-NAME) and stimulated by supplementing the diet with L-arginine (L-Arg). The aim of this study was to investigate the role of NO on gastric mucosal injury induced by ASA. Materials and Methods: Male Sprague-Dawley rats were divided into seven groups: control, ASA, ASA+L-NAME, ASA+L-Arg, ASA+L-Arg+L-NAME, only L-NAME, and only L-Arg groups. After administration of the drugs, the rats were decapitated and their stomachs were removed and fixed in 10% neutral-buffered formalin solution. Results: Mucosal erosion, intramucosal hemorrhage, inflammatory cell infiltration, gland cell detachment, and necrosis were observed in the ASA group. It was demonstrated that L-Arg administration decreased the gastric mucosal injury, whereas L-NAME administration increased the extent and severity of the gastric injury induced by ASA. L-Arg or L-NAME administration alone did not affect gastric mucosa. Conclusions: We concluded that NO may have protective effects on gastric mucosal injury induced by ASA.