牛磺酸镁配合物对乌头碱诱发心律失常大鼠心肌细胞钙通道的影响

目的研究牛磺酸镁配合物(TMCC)对乌头碱诱发心律失常大鼠心肌细胞L型钙电流(I_(Ca,L))的影响。方法酶解法分离大鼠单个心室肌细胞,乌头碱诱导大鼠心律失常模型,胺碘酮作为阳性对照,100、200和400μmol·L~(-1)TMCC作用于心肌细胞。应用全细胞膜片钳技术记录心室肌细胞I_(Ca,L)的变化。结果 400μmol·L~(-1)TMCC显著增加大鼠正常心肌细胞I_(Ca,L),胺碘酮则使之减小。1μmol·L~(-1)乌头碱使I_(Ca,L)电流密度由(4.3±1.6)pA·pF~(-1)增加到(6.4±1.9)pA·pF~(-1)(p<0.01),400μmol·L~(-1)TMCC能显著降低乌头碱诱导的I_(Ca,L)增加。胺碘酮则能使之恢复为(3.7±1.4)pA·pF~(-1)。结论 400μmol·L~(-1)TMCC能增加正常细胞的I_(Ca,L),对钙内流有促进作用,并可减少乌头碱诱导的心律失常大鼠心肌细胞异常增加的电流。

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

AIM To investigate the effects of taurine-magnesium coordination compound(TMCC) on calcium current(I_(Ca,L)) in rat ventricular myocytes of arrhythmia induced by aconitine.METHODS Whole-cell patch clamp was used to record I_(Ca,L) in normal cardiomyocytes and single rat ventricular cardiomyoeyte of arrhythmia induced by aconitine.Amiodarone served as a positive control.TMCC(100,200 and 400μmol·L~(-1)) was acted on the ventricular cardiomyocytes.RESULTS In ventricular cardiomyocytes of rat,I_(Ca,L) was increased by TMCC 400μmol·L~(-1),while decreased by amiodarone.I_(Ca,L) was increased from(4.3±1.6) pA·pF~(-1) to(6.4±1.9) pA·pF~(-1)(P<0.01) by 1μmol·L~(-1) aconitine.400μmol·L~(-1) TMCC can restore I_(Ca,L) significantly.Amiodarone can restore it to(3.7±1.4) pA·pF~(-1).CONCLUSION 400μmol·L~(-1) TMCC increases I_(Ca,L) of ventricular cardiomyocytes.The effects of TMCC on I_(Ca,L) may be one of its antiarrhythmic mechanisms.