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研究利多卡因对克隆h ERG钾通道的作用,探讨其对心脏电生理的影响。利用全细胞膜片钳技术和Western blot技术,观察利多卡因对稳定表达h ERG钾通道的HEK 293细胞h ERG电流和蛋白表达的影响,同时观察利多卡因对离体兔心脏心电图的影响。结果显示,利多卡因在0.3~1 000μmol·L~(-1)内呈浓度依赖性抑制h ERG电流,IC50值为88.63±7.99μmol·L~(-1);抑制作用在大于20 m V电压下更明显,不影响通道激活曲线,但具有频率依赖性特点;慢性孵育利多卡因不影响h ERG蛋白的表达;利多卡因对QTc间期没有明显影响,但浓度大于100μmol·L~(-1)可减慢心率,延长PR间期以及QRS波。结果表明,尽管利多卡因在较高浓度下具有潜在的h ERG电流抑制作用,但并不引起QTc间期延长。
To investigate the effect of lidocaine on the ERG potassium channel of cloned h and explore its effect on cardiac electrophysiology. The effects of lidocaine on h ERG current and protein expression in hTERG-positive HEK 293 cells stably expressing h ERG were observed by whole-cell patch clamp technique and Western blotting. Meanwhile, the effect of lidocaine on isolated rabbit heart electrocardiogram was observed. The results showed that lidocaine inhibited h ERG currents in a concentration-dependent manner from 0.3 to 1 000 μmol·L -1 with an IC50 value of 88.63 ± 7.99 μmol·L -1 and an inhibitory effect at more than 20 mV The voltage is more obvious, does not affect the channel activation curve, but with a frequency-dependent characteristics; chronic incubation of lidocaine h ERG protein expression; lidocaine QTc interval had no significant effect, but the concentration greater than 100μmol·L ~ ( -1) can slow heart rate, prolong PR interval and QRS wave. The results showed that, although lidocaine had potential h ERG current inhibition at higher concentrations, it did not cause QTc interval prolongation.