Background Some clinical trials have shown statins have anti-arrhythmic effects and can improve clinical results. But its mechanism is unclear.
Objective observing the effects of atorvastatin on transient sodium currents in rat normal/simulated ischemia/reperfusion ventricular cell.
Methods Taking whole-cell patch clamp method to record INa and measuring the expression level of SCN5A by western blot technique of simulated ventricular ischemia /reperfusion cell.
Results The short-time effects of atorvastatin on the rat normal and simulated ischemia ventricular peak INa were inhibited about 25% (p<0.05), and after elution, inhibition disappeared. However 15 min after simulated ischemia atorvastatin inhibited the INa decreasing progress. In simulated reperfusion status, INa reduced and atorvastatin inhibited the reduction degree, while INa of the atorvastatin and wortmannin combination group had no difference with which of reperfusion group (p>0.05). The expression level of SCN5A had the almost same changes with INa.
Conclusion (1) The short time (3 min) effect of Atorvastatin in INa of the normal and simulated ischemia rat ventricular myocytes is inhibition, similar to sodium channel blockers. (2) Atorvastatin can protect the decrease of INa in the status of simulated long-time (>15 min) ischemia/reperfusion. (3) Effects of Atorvastatin in the status of simulated ischemic/reperfusion can be partly overcome by Wortmannin, which means atorvastatin can affect INa and the expression level of SCN5A through the way of RISK signal pathway especially of PI3K.