中文摘要：

目的观察哇巴因和乌头碱对豚鼠和大鼠心肌细胞钠电流的作用，探讨二药诱发心律失常的机制。方法用全细胞膜片钳技术分别记录豚鼠和大鼠单个心肌细胞钠电流。结果在-40mV电压下，哇巴因5μmol／L使INa从（-48．3±8．9）pA/pF减少到（-22．6±5．6）pA/pF（抑制60．1％，n=5，P〈0．01）；乌头碱1μmol／L使INa从（-21．8±5．8）pA/pF增加到（-67．3±7．8）pA/pF（增加208．7％，n=4，P〈0．01）。结论哇巴因抑制豚鼠心肌细胞钠电流而乌头碱增加大鼠心肌细胞钠电流。不论是抑制还是促进钠电流，二药均使离子通道失衡，这是其诱发心律失常的重要机制。

英文摘要：

Objective To observe the effects of ouabain and aconitine on INa of isolated guinea pig and rat ventricular myocytes. To discuss the arrhythmic mechanisms of the two drugs. Methods Whole cell patch clamp mode was used to record sodium current of isolated single ventricular myocytes. Results 5μmol/L ouabain inhibited INa from （ -48.3±8.9 ） pA/pF to （ -22.6±5.6） pA/pF at -40mV （inhibition rate of 60.1%,n=5,P〈0.01 ）. 1μmol/L aconitine increased INa from （ -21.8 ± 5.8）pA/pF to （-67.3±7.8） pA/pF at -40mV（increase rate of 208.7%,n =4, P 〈 0.01）.Conclusion Ouabain can decrease sodium current and aconitine can increase sodium current. Either decrease or increase of INa, these two drugs could destroy the balance of ion channels in the heart which is the important mechanism of arrhythmia.