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机构地区:[1]华中科技大学协和医院心内科 [2]广州市天河区卫生局
出 处:《临床心血管病杂志》2007年第2期125-127,共3页Journal of Clinical Cardiology
摘 要: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。Objective: To study the molecular mechanism of benzylterahydropalmatine(BTHP) in counteracting arrhythmia. Method: To compare BTHP with classical class Ⅲ antiarrhythmic drug-amiodarone in blocking the outward potassium current of Kvl. 2 channel expressed on the membrane of xenopus oocytes. Result: Both BTHP and amiodarone could block the outward potassium current of Kv1.2. In the range of concentration from 10^-3 to 10 mmol/L, the blocking ability enhanced and there was no significant difference between them. Conclusion: BTHP can block the outward potassium current of Kv1. 2, which is one the of mechanisms for its counteracting arrhythmia.
分 类 号:R541.7[医药卫生—心血管疾病]
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