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Effects of taurine-magnesium coordination compound on ionic channels in rat ventricular myocytes of arrhythmia induced by ouabain

机译:牛磺酸-镁配位化合物对哇巴因致心律失常大鼠心室肌细胞离子通道的影响

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Taurine-magnesium coordination compound (TMCC) has anti-arrhythmic effects. The aim of the present study was to explore the targets of the anti-arrhythmic effect of TMCC and the electrophysiological effects of TMCC on ouabain-induced arrhythmias in rat ventricular myocytes. Sodium current (I Na), L-type calcium current (I ca, L), and transient outward potassium current (I to) were measured and analyzed using whole-cell patch-clamp recording technique in normal rat cardiac myocytes and rat ventricular myocytes of arrhythmia induced by ouabain. In isolated ventricular myocytes, I Na and I to were blocked by TMCC (100, 200, 400 μM) in a concentration-dependent manner, and the effects of TMCC (400 μM) were equal to that of amiodarone. However, I ca, L was moderately increased by TMCC (400 μM) while significantly decreased by amiodarone. Ouabain (5 μM) significantly decreased sodium, L-type calcium, and transient outward potassium currents. TMCC (100 μM) relieved abnormal sodium currents induced by ouabain through facilitation of steady-state inactivation. TMCC (200 and 400 μM) relieved abnormal L-type calcium currents induced by ouabain through facilitation of steady-state activation and retardation of steady-state inactivation. TMCC failed to further inhibit abnormal transient outward potassium currents induced by ouabain. However, amiodarone inhibited the decreasing sodium, L-type calcium, and transient outward potassium currents further. These data suggest that I Na, I ca, L, and I to may be the targets of the antiarrhythmic effect of TMCC, which can antagonize ouabain-induced changes of ionic currents in rat ventricular myocytes.
机译:牛磺酸-镁配位化合物(TMCC)具有抗心律失常作用。本研究的目的是探讨TMCC的抗心律失常作用和TMCC对哇巴因引起的心室肌心律失常的电生理作用。使用全细胞膜片钳记录技术对正常大鼠心肌细胞和大鼠心室肌细胞中的钠电流(I Na),L型钙电流(I ca,L)和瞬时向外钾电流(I to)进行测量和分析哇巴因引起的心律失常。在分离的心室肌细胞中,I Na和I to以浓度依赖的方式被TMCC(100、200、400μM)阻断,并且TMCC(400μM)的作用与胺碘酮相同。但是,TMCC(400μM)使I ca,L适度增加,而胺碘酮则显着降低。瓦巴因(5μM)显着降低了钠,L型钙和瞬时外向钾电流。 TMCC(100μM)通过促进稳态失活缓解了哇巴因引起的异常钠电流。 TMCC(200和400μM)通过促进稳态激活和延迟稳态失活来缓解哇巴因引起的异常L型钙电流。 TMCC不能进一步抑制哇巴因引起的异常的瞬时向外钾电流。但是,胺碘酮可进一步抑制钠,L型钙和瞬时向外钾电流的减少。这些数据表明,I Na,I ca,L和I to可能是TMCC的抗心律不齐作用的靶标,后者可拮抗哇巴因诱导的大鼠心室肌细胞离子电流变化。

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