牛磺酸镁对哇巴因致豚鼠心肌细胞心律失常模型钙离子通道的作用机制分析

Effect of Taurine-Magnesium Coordination Compound on Calcium Channel in Rat Cardiomyocytes of Arrhythmia Induced by Ouabain

目的:研究牛磺酸镁(TMCC)对哇巴因致豚鼠心肌细胞心律失常模型钙离子通道的作用机制。方法:运用全细胞膜片钳技术分别记录TMCC和胺碘酮对正常心肌细胞和哇巴因导致的心律失常心肌细胞模型钙离子通道的作用。结果:5μmol/L哇巴因使心肌细胞钙离子通道电流(ICa-L)减小。200和400μmol/L可以明显使I Ca-L恢复。24.26μmol/L胺碘酮使I Ca-L进一步减少(P>0.05)。结论:400μmol/L TMCC可以明显加大正常细胞的I Ca-L,起到促进钙内流的作用,并且增强哇巴因致豚鼠心律失常心肌细胞异常减少的电流。

Objective： To investigate the antiarrhythmic mechanism of taurine-magnesium coordination compound （TMCC） on L-type calcium current （ICa-L） in rat ventricular myocytes of arrhythmia induced by oubain. Methods： Whole-cell patch clamp was used to record ICn-L in normal cardiomyocytes and single rat ventricular cardiomyocytes of arrhythmia induced by ouabain. Results： In rat ven- tricular cardiomyocytes, IC-L was increased by TMCC （400μmol/L）, and was decreased by amiodarone （P〈0.05）. IC-L was decreased by 5 μmol/L ouabain. TMCC （200,400μmol/L） restored ICa-L significantly in rat ventricular myocytes of arrhythmia induced by oubain. Furthermore, 24.26 μmol/L of Amiodarone can luther decreased ICa-L （P〈0.05）. Conclusion： TMCC （400μmol/L） can increase ICa-L in normal cardiomyocytes, and also significantly increases ICa-L in single rat ventricular cardiomyocytes of arrhythmia induced by ouabain.