论文部分内容阅读
采用全细胞电压钳技术，以确定青蒿素对分离的豚鼠心室肌细胞和狗的浦肯野纤维钾离子电流的影响．在豚鼠心室肌细胞，青蒿素呈浓度依赖关系显著降低内向整流钾电流〔ＩＫ１，膜电位为－１００ｍＶ时，ＩＣ５０为（７．２±０．８）μｍｏｌ·Ｌ－１〕，且这种抑制作用不呈现频率依赖性．５０μｍｏｌ·Ｌ－１的青蒿素降低延迟整流钾电流（ＩＫ）：时间依赖性外向钾电流（ＩＫｓｔｅｐ）在膜电位为＋４０ｍＶ时减少（３８±１０）％．尾电流步阶分析提示，ＩＫ的快组分（ＩＫｒ）和慢组分（ＩＫｓ）均被抑制．在犬浦肯野纤维，青蒿素明显抑制瞬时外向钾电流（Ｉｔｏ），ＩＣ５０为（４．２±０．３）μｍｏｌ·Ｌ－１．实验结果表明，青蒿素以相似效率抑制ＩＫ１，Ｉｔｏ和ＩＫ，其抗心律失常作用可能与抑制ＩＫ１，Ｉｔｏ，ＩＫｒ和ＩＫｓ有关．
Whole-cell voltage-clamp technique was used to determine the effect of artemisinin on potassium currents in Purkinje fiber isolated from isolated guinea pig ventricular myocytes and dogs. In guinea pig ventricular myocytes, artemisinin significantly reduced the inward rectifier potassium current [IK1 (IC50, (7.2 ± 0.8) μmol·L-1] in a concentration-dependent manner The inhibitory effect does not appear to be frequency-dependent. Artemisinin at 50 μmol·L -1 decreased delayed rectifier potassium current (IK): the time-dependent outward potassium current (IKstep) decreased by (38 ± 10)% at a membrane potential of +40 mV. Tail current step analysis suggested that both IKr and IKs of IK were inhibited. In canine Purkinje fiber, artemisinin significantly inhibited the transient outward potassium current (Ito) with an IC50 of (4.2 ± 0.3) μmol·L-1. The experimental results show that artemisinin can inhibit IK1, Ito and IK with similar efficiency, and its antiarrhythmic effect may be related to the inhibition of IK1, Ito, IKr and IKs.