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目的:研究苄基四氢巴马汀(BTHP)抗心律失常作用的分子机制。方法:比较BTHP和经典Ⅲ类抗心律失常药胺碘酮对卵母细胞膜上表达的Kv1.2通道的外向钾电流的阻滞作用。结果:BTHP和胺碘酮对Kv1.2通道的外向钾电流均有阻滞作用,在10-3～10mmol/L浓度范围内,对电流的阻滞作用增强,二者相比,差异无统计学意义。结论:BTHP能够阻滞Kv1.2通道的外向钾电流,这是其抗心律失常作用的分子机制之一。
AIM: To investigate the molecular mechanism of anti-arrhythmic effects of benzyltetrahydropalmatine (BTHP). METHODS: A comparison of the blockade of outward potassium currents in Kv1.2 channels expressed on oocyte membranes by BTHP and class III antiarrhythmic amiodarone was performed. Results: Both BTHP and amiodarone blocked the outward potassium current in Kv1.2 channel, and the current blocking effect was enhanced in the concentration range of 10-3 ~ 10mmol / L. There was no statistical difference between the two Significance of learning. CONCLUSION: BTHP can block the outward potassium channel of Kv1.2 channel, which is one of the molecular mechanisms of anti-arrhythmic effect.