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Objective:To investigate the effect of atorvastatin on serum oxidative stress andN-terminal brain natriuretic peptide expression in rats.Methods:A total of40 healthy maleSD rats were randomly divided into the sham group(GroupA,n=10, saline5 mL/d), ischemia-reperfusion group(GroupB,n=10, saline5 mL/d), atorvastatin group(GroupC,n=10, atorvastatin20 mg/kg?d), atorvastatin+N-amino-arginine group(GroupD,n=10, atorvastatin20 mg/kg?d+N-amino arginine15 mg/kg).Myocardial ischemia-reperfusion rat model was established after3 days of gavage.N-amino arginine15 mg/kg was given by tail vein injection15 min before ischemia. After reperfusion, enzymology indicators such us creatine kinase(CK) and lactate dehydrogenase and the oxidative stress parameters such as nitric oxide(NO), malondialdehyde(MDA) and total superoxide dismutase(TSOD), andn-terminal pro-brain natriuretic peptide(NT-proBNP) expression was detected by immunohistochemistry.Results:LDH andCK levels of groupA were significantly lower than the other three groups, and groupB was the highest.There was significant difference between groupB and groupC(P<0.05), and no significant difference between groupB and groupD(P>0.05).MDA levels in groupB were significantly higher than the other three groups. The lowest was groupA, followed by groupC, the difference among groups was significantly (P<0.05).TSOD andNO levels in groupB was the lowest, the level in groupA was the highest, followed by groupC, the difference among groups was significant(P<0.05).NT-proBNP level in groupB was significantly higher than the other three groups, the lowest was groupA, followed by groupC, the difference among groups was significant(P<0.05).Conclusions:Atorvastatin has a protective effect on the myocardial injury in the myocardial ischemia and reperfusion rats.It can increaseNO synthesis and decreaseMDA content, increase serumTSOD activity and the oxidative stress effect, meanwhile protect myocardial cells and reduce myocardial injury.