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中文摘要：
目的观察奎尼丁对缺血心肌细胞钠电流的作用，探讨奎尼丁致心律失常发生的离子机制。方法采用大鼠冠状动脉左前降支结扎，制备心肌梗死（心梗）实验动物模型，每日给予奎尼丁（10mg／kg）灌胃，连续3个月．膜片钳技术观察奎尼丁对缺血后心肌细胞钠电流的作用。结果长期应用奎尼丁可导致心梗大鼠死亡率上升（Х^2=4．28，P〈0．05）。膜片钳测定结果表明，在刺激电压为-30mV时，奎尼丁组心肌细胞钠电流幅度为-（1284±129）pA，明显低于对照组的-（1985±204）pA，两组比较差异有统计学意义（t=3．015，P〈0．01）。结论奎尼丁对缺血后的心肌细胞钠电流具有较强的抑制作用；心肌缺血后，由于奎尼丁对不同离子电流的抑制作用不同，导致离子电流失衡，是奎尼丁致心律失常的离子机制。
英文摘要：
Objective To observe the effect of quinidine on sodium current of ventricular myocytes from post-ischaemic rats so as to explore the proarrhythmic mechanisms of quinidine. Methods The left anterior descending （LAD） coronary artery was ligated to establish the ischemia heart model in Wistar rats. Quinidine （10 mg·kg^-1·d^-1） was administered to rats with coronary occlusion for 3 months. Whole-cell patch clamp techniques were used to record sodium current （INa）. Results The morbidity rate of post-ischemic rats was increased by chronic application of quinidine. At the test potential of - 30 mV, the sodium current amplitude of ventricular myocytes from quinidine-treated group was significantly decreased to - （1 284±129） pA from - （1 985±204） pA in ischemic group （t = 3.015,P 〈 0.01）. Conclusions Sodium current was sensitive to quinidine even in post-ischemic heart. The different effects of quinidine on different currents in post-ischemic heart resulted in imbalance of ionic currents of ischemic heart. That may be the ionic mechanism of proarrhythmic effect of chronic application of quinidine.
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