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.