Objective To investigate the effects of simvastatin on membrane ionic currents in left ventricular myocytes after acute myocardial infarction (AMI,so as to explore the ionic mechanism of statin treatment for antiarrhythmia.Methods Fourty-five New Zeland rabbits were randomly divided into three groups:AMI group,simvastatin intervention group (statin group) and sham-operated control group (CON).Rabbits were infarcted by ligation of the left anterior descending coronary artery after administration of oral simvastatin 5 mg·kg~(-1)·d~(-1) (Statin group) or placebo (AMI group)for 3 days.Twenty-four hours later,single ventricular myocytes were isolated enzymatically from the epicardial zone of the infracted region.Whole cell patch clamp technique was used to record membrane ionic currents,including sodium current (I_(Na)),L-type calcium current (I_(Ca-L)) and transient outward potassium current (I_(to)).Results①There was no significant difference in serum cholesterol concentration among three groups.②The peak I_(Na) current density (at-30 mV) was significantly decreased in AMI group (-23.26±5.18) compared with CON (-42.78±5.48,P<0.05),while it was significantly increased in Statin group (-39.23±5.45) compared with AMI group (P<0.01);The peak I_(Ca-L) current density (at 0 mV) was significantly decreased in AMI group (-3.23±0.91) compared with CON (-4.56±1.01,P<0.05),while it was significantly increased in Statin group (- 4.18±0.95) compared with AMI group (P<0.05);The I_(to) current density(at +60 mV) was significantly decreased in AMI group(10.41±1.93)compared with CON (17.41±3.13,P<0.01),while it was significantly increased in Statin group(16.21±2.42)compared with AMI group (P<0.01).Conclusions AMI induces significant down-regulation of I_(Na),I_(Ca-L) and I_(to).Pretreatment with simvastatin could attenuate this change without lowering the serum cholesterol level,suggesting that simvastatin reverse this electrical remodeling,thus contributing to the ionic mechanism of statin treatment for antiarrhythmia. Objective To investigate the effects of simvastatin on membrane ionic currents in left ventricular myocytes after acute myocardial infarction (AMI, so as to explore the ionic mechanism of statin treatment for antiarrhythmia. Methods Fourty-five New Zeland rabbits were randomly divided into three groups: AMI group, simvastatin intervention group (statin group) and sham-operated control group (CON). Rabbits were infarcted by ligation of the left anterior descending coronary artery after administration of oral simvastatin 5 mg · kg -1 · d ~ (- 1) (Statin group) or placebo (AMI group) for 3 days.Twenty-four hours later, single ventricular myocytes were isolated enzymatically from the epicardial zone of the infracted region. Hole cell patch clamp technique was used to record membrane ionic currents, including sodium current (I_ (Na)), L-type calcium current (I_ (Ca-L)) and transient outward potassium current (I_ (to)) Results ① There was no significant difference in serum cholesterol concentration among t hree groups.②The peak I_ (Na) current density (at-30 mV) was significantly decreased in AMI group (-23.26 ± 5.18) compared with CON (-42.78 ± 5.48, P <0.05), while it was significantly increased in Statin The peak I_ (Ca-L) current density (at 0 mV) was significantly decreased in AMI group (-3.23 ± 0.91) compared with CON (-4.56 ± 1.01, P <0.05), while it was significantly decreased in AMI group (- 4.18 ± 0.95) compared with AMI group (P <0.05) (10.41 ± 1.93) compared with CON (17.41 ± 3.13, P <0.01), while it was significantly increased in Statin group (16.21 ± 2.42) compared with AMI group (P <0.01) .Conclusions AMI induces significant down- I_ (Na), I_ (Ca-L) and I_ to .Pretreatment with simvastatin could attenuate this change without lowering the serum cholesterol level, suggesting that simvastatin reverse this electrical remodeling, thus contributing to the ionic mechanism of sstatin treatment for antiarrhythmic.