Objective:To investigate the beneficial effects of Simvastatin on cardiac remodeling and cardiac dysfunction after myocardial infarction and its possible mechanisms.Methods:Simvastatin was administered to the rats with myocardial infarction rats by left anterior descending coronary artery ligation.After 8 weeks

cardiac remodeling was observed through right ventricular weight index （RVWI）

and left ventricular weight index （LVWI）.Changes in hemodynamics were observed.The activity of nitric oxide synthase （NOS） and inducible nitric oxide synthase （iNOS） in left ventricle and serum were measured.Results:In the rat model of myocardial infarction RVWI

LVWI increased and activity of NOS and iNOS in ventricle and serum decreased（P

<

0.01）.Left ventricular systolic pressure（LVSP）

the ventricular pressure rise ratio during systolic period(+dp/dt

max

)

the ventricular pressure rise decay ratio during diastolic period (-dp/dt

max

) decreased（P

<

0.01） and left ventricular end diastolic pressure （LVEDP） rised（P

<

0.01）.Simvastatin attenuated RVWI

LVWI （each P

<

0.01） and NOS iNOS activity increased （P

<

0.01）.APS APD LVSP +dp/dt

max

-dp/dt

max

rised （P

<

0.01） and LVEDP decreased （P

<

0.01）.Conclusion:Simvastatin improves cardiac remodeling and cardiac dysfunction after myocardial infraction.And the improvement of NO availability may be one of the mechanisms.