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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。
Objective To observe the effects of ouabain and aconitine on sodium currents in guinea pig and rat cardiomyocytes and to explore the mechanism of two drugs inducing cardiac arrhythmia. Methods Whole-cell patch-clamp technique was used to record the sodium currents of single cardiomyocytes in guinea pig and rat respectively. Results ouabain was reduced from (-48.3 ± 8.9) pA / pF to (-22.6 ± 5.6) pA / pF (60.1% inhibition, n = 5, P <0.01) at a dose of -40 mV. Aconitine 1 μmol / L increased INa from (-21.8 ± 5.8) pA / pF to (-67.3 ± 7.8) pA / pF (208.7% increase, n = 4, P <0.01). Conclusion ouabain can inhibit sodium currents in guinea pig cardiomyocytes while aconitine increases sodium current in rat cardiomyocytes. Whether inhibition or promotion of sodium current, the two drugs are ion channel imbalance, which is an important mechanism of its induced arrhythmia.