牛磺酸镁对乌头碱致大鼠心肌细胞心律失常模型钠离子通道的影响  

Effects of taurine-magnesium coordination compound on sodium channel in rat cardiomyocytes of arrhythmia induced by aconitine

作　　者：汪玲芳[1] 尹永强[1] 赵临[1] 吴红[1] 康毅[1] 娄建石[1] 

机构地区：[1]天津医科大学药理学教研室,天津300070

出　　处：《中国药理学通报》2010年第5期611-614,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No30672458)

摘　　要：目的研究牛磺酸镁配合物(taurine magnesium coordi-nation compound,TMCC)对乌头碱所致大鼠心室细胞心律失常模型的钠电流变化的影响,探讨其抗心律失常的作用机制。方法酶解法分离大鼠单个心室肌细胞,应用全细胞膜片钳技术记录不同浓度TMCC及胺碘酮对正常细胞及乌头碱所致大鼠单个心室肌细胞心律失常模型INa变化。结果TMCC对正常细胞INa呈浓度依赖性抑制作用。1μmol.L-1乌头碱使钠电流从(45.56±1.96)pA/pF增加到(59.19±11.49)pA/pF(n=5,P<0.01)。24.24μmol.L-1胺碘酮使电流减小到(34.23±1.33)pA/pF(n=5,P<0.01)。TMCC(100,200,400μmol.L-1)对乌头碱所致的细胞模型INa具有恢复作用,分别恢复为(51.61±5.96)pA/pF,(40.91±6.73)pA/pF,(41.50±5.50)pA/pF。胺碘酮则使之恢复为(40.22±1.47)pA/pF。结论TMCC能恢复乌头碱增大的钠电流,作用与胺碘酮相当,TMCC对钠电流的抑制作用可能是其发挥抗心律失常的机制之一。Aim To investigate the antiarrhythmic mechanism of taurine-magnesium coordination compound on sodium current in single rat ventricular myocytes of arrhythmia induced by aconitine.Methods Whole-cell patch clamp was used to record INa in normal cardiomyocytes and single rat ventricular cardiomyocytes of arrhythmia induced by aconitine.Results In ventricular cardiomyocytes of rat,INa was blocked by 100-400 μmol·L^-1 TMCC in a concentration-dependent manner.INa was increasd from（45.56±1.96）pA/pF to（59.19±11.49）pA/pF by 1 μmol·L^-1 aconitine,while decreased to（34.23±1.33）pA/pF by 24.24 μmol·L-1 amiodarone.TMCC（100,200,400 μmol·L^-1）could restore INa to（51.61±5.96）pA/pF,（40.91±6.73）pA/pF,（41.50±5.50）pA/pF respectively.Amiodarone could restore INa to（40.22±1.47）pA/pF.Conclusions TMCC can restore INa,which is increased by aconitine,and the effect is equal to that of amiodarone.TMCC blocks INa of ventricular cardiomyocytes,which may be one of its antiarrhythmic mechanisms.

关 键 词：牛磺酸镁 乌头碱 心律失常 钠通道 全细胞膜片钳 胺碘酮 

分 类 号：R-332[医药卫生] R322.11