Abstract:Objective: To observe influence of matrine on sodium channel current(INa)of ventricle muscle cells in guinea pigs and to discuss its antiarrhythmic mechanism. Method: Guinea pigs were randomly divided into control group, aconitine group and matrine group. Each group included eight cases. Aconitine group was treated with 50 μmol·L-1 aconitine perfusion 10 min while matrine group was treated with 10,50,100 μmol·L-1 matrine based on aconitine group. The whole-cell patch clamp technique was used to record INacurrent of single ventricle muscle cell and then to design figures of INa current density. Result: Aconitine(50 μmol·L-1) could significantly amplify INa current(-92.62±6.5) pA/pF (compared with control group(-66.24±4.8,P<0.05). Based on aconitine-induced arrhythmia, matrine(10 μmol·L-1) had no significant effects on INa current,however, matrine(50 μmol·L-1) could significantly reduce INa current(-49.21±5.1) pA/pF (compared with aconitine group, P<0.05),but when the dose of matrine was kept increasing, the effect of reducing INa current of matrine were getting weak, and at the level of 100 μmol·L-1, matrine could slightly amplify INa current (compared with control group, P>0.05). Conclusion: Matrine could restrict INa current in dose-dependent manner, and high dose of matrine could make this effect of restriction weak, so matrine has a two-way, modest and lasting regulation effect which probably was one of its antiarrhythmic mechanisms.