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目的：研究长春西汀对心肌细胞钠电流的作用．方法：用全细胞膜片箝技术记录大鼠心肌细胞钠电流．结果：长春西汀可逆性抑制心肌细胞钠电流的作用为剂量依赖性和电压依赖性，但未发现频率或使用依赖性．长春西汀１０－８０μｍｏｌ·Ｌ－１，对钠电流的抑制作用为１３％±２％至７５％±６％．半数抑制浓度ＩＣ５０值（９５％可信限）为３６４（２８１－４７１）μｍｏｌ·Ｌ－１．在膜电位以１０ｍＶ的间隔从－９０ｍＶ阶梯状去极化至＋４０ｍＶ时，抑制作用呈逐渐增加的趋势，约在０ｍＶ左右达到最大抑制．长春西汀对钠通道的稳态激活和失活过程的影响，可使钠窗电流（缓慢失活的钠电流）减少．结论：长春西汀抑制大鼠心肌细胞的钠电流
Objective: To study the effect of vinpocetine on sodium current in cardiomyocytes. Methods: Whole-cell patch clamp technique was used to record rat cardiomyocyte sodium current. RESULTS: Vinpocetine reversibly inhibited cardiomyocyte sodium currents in a dose-dependent and voltage-dependent manner, but no frequency or dependence was found. Vinpocetine 10-80μmol·L-1, the inhibition of sodium current of 13% ± 2% to 75% ± 6%. IC50 value (95% confidence limit) was 36.4 (28.1-47.1) μmol·L-1. When the membrane potential was depolarized from -90 mV stepwise to +40 mV at 10 mV intervals, the inhibition tended to increase gradually, reaching maximum suppression around 0 mV. The effect of vinpocetine on the steady-state activation and inactivation of sodium channels can reduce the sodium window current (slow inactivation of sodium currents). Conclusion: Vinpocetine inhibits sodium currents in rat cardiomyocytes