Objective: To investigate the effect of atorvastatin on serum oxidative stress and N-terminal brain natriuretic peptide expression in rats. Methods: A total of 40 healthy male SD rats were randomly divided into the sham group (Group A, n=10, saline 5 mL/d), ischemia-reperfusion group (Group B, n=10, saline 5 mL/d), atorvastatin group (Group C, n=10, atorvastatin 20 mg/kg.d, atorvastatin +N-amino-arginine group (Group D, n=10, atorvastatin 20 mg/kg.d + N-amino-arginine 15 mg/kg). Myocardial isehemia-reperfusion rat model was established after 3 days of gavage. N-amino arginine 15 mg/kg was given by tail vein injection 15 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), and a terminal pro brain natriuretic peptide (NT-proBNP) expression was detected by immunohistochemistry. Results: LDH and CK levels of group A were significantly lower than the other three groups, and group B was the highest. There was significant difference between group B and group C (P0.05). MDA levels in group B were significantly higher than the other three groups. The lowest was group A, followed by group C, the difference among groups was significantly (P<0.05). TSOD and NO levels in group B was the lowest, the level in group A was the highest, followed by group C, the difference among groups was significant (P<0.05). NT-proBNP level in group B was significantly higher than the other three groups, the lowest was group A, followed by group C, 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 increase NO synthesis and decrease MDA content, increase serum TSOD activity and the oxidative stress effect, meanwhile protect myocardial cells and reduce myocardial injury.