RESUMO
AIM: To investigate the effects of anisodamine on the sodium current (I_(Na)) in left ventricular myocytes of rabbit heart undergoing ischemia/reperfusion, so as to explore the cellular (ionic) basis of anisodamine treatment for antiarrhythmia. METHODS: Forty-five rabbits were randomly divided into three groups: ischemic/reperfusion group (I/R), anisodamine intervention group (Ani+I/R) and sham-operated control group (CON). Anesthetized rabbits were subjected to 30 min ischemia by ligation of the left anterior descending coronary artery and 60 min reperfusion. The animals in Ani group were injected with anisodamine at a dose of 5 mg/kg via femoral vein 1 min before operation. The incidence of ventricular arrhythmia was observed. Single ventricular myocytes were isolated enzymatically from the epicardial zone of the infracted region derived from the hearts in I/R, Ani+I/R group and the same anatomy region in CON. Whole cell patch clamp technique was used to record I_(Na). RESULTS: Anisodamine intervention decreased the incidence and duration of ventricular arrhythmia by reperfusion compared to I/R group, resulting in significant decrease in the scores of arrhythmia (2.6±0.7 vs 3.6±0.8, P<0.05). The peak I_(Na) current density (at-30 mV) was significantly decreased in I/R group (-22.46±5.32 pA/pF, n=12) compared to CON (-42.78±5.48 pA/pF, n=16, P<0.01), while it was significantly increased in Ani+I/R group (-38.89±5.24 pA/pF, n=13) compared to I/R group (P<0.01). CONCLUSION: Anisodamine has the ability to reduce the occurrence of ventricular arrhythmia. Ischemia-reperfusion induces significant down-regulation of I_(Na), while pretreatment with anisodamine attenuates this change, suggesting that anisodamine reverses this electrical remodeling, which may be partly responsible for its antiarrhythmia effects.
RESUMO
Objective To investigate the effects of simvastatin on membrane ionic currents in left ventricular myocytes after acutemyocardial infarction(AML.so as to explore the ionic mechanism of statin treatment for antiarrhythmia.Methods Fourty-five NewZeland rabbits were randomly divided into three groups:AMI group,simvastatin intervention group(statin group)and sham-operatedcontrol group (CON).Rabbits were infarcted by ligation of the left anterior descending coronary artery after administration of oralisolated enzymatically from the epicardial zone of the infractcd region.Whole cell patch clamp technique was used to record mmbranewas significantly decreased in AMI group(-23.26+5.1 8)compared with CON(-42.78±5.48,P＜0.05),while it was significantlyincreased in Stating roup(-39.23±5.45)compared with AMI group(P＜0.01);The peak Ica-L current density(at 0 mV) was significantlydecreased 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 Ito 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 withattenuate this change without lowering the serum cholesterol level,suggesting that simvastatin reverse this electrical remodeling thuscontributing to the ionic mechanism of statin treatment for antiarrhythmia.