Zhao L, Lou J-S, Kang Y
Department of Pharmacology, Tianjin Medical University, Tianjin, China.
Drug Res (Stuttg). 2013 Apr;63(4):185-91. doi: 10.1055/s-0033-1334881. Epub 2013 Mar 13.
Because of the known anti-arrhythmic effects of taurine-magnesium coordination compound (TMCC), the aim of the present study was to explore the electrophysiological effects of TMCC on hypoxia/reoxygenation (H/R)-induced arrhythmias in rat ventricular myocytes. Sodium current (I Na), the L-type calcium current (I Ca,L), and the transient outward potassium current (I to) were evaluated using whole-cell patch-clamp recordings in rat ventricular myocytes following H/R injury. The H/R group significantly decreased sodium currents, while L-type calcium currents and transient outward potassium currents was significantly increased (all p<0.01). TMCC (200 and 400 μM) prevented abnormal sodium currents induced by H/R by inhibiting steady-state inactivation. It also counteracted abnormal L-type calcium currents induced by H/R by inhibiting steady-state activation and facilitating steady-state inactivation. In addition, it mitigated abnormal transient outward potassium currents induced by H/R by inhibiting steady-state activation. TMCC prevents H/R-induced arrhythmias in rat ventricular myocytes by modifying ion channel function.
由于已知牛磺酸镁配位化合物（TMCC）具有抗心律失常作用，本研究旨在探讨TMCC对大鼠心室肌细胞缺氧/复氧（H/R）诱导的心律失常的电生理效应。在H/R损伤后的大鼠心室肌细胞中，使用全细胞膜片钳记录评估钠电流（I Na）、L型钙电流（I Ca,L）和瞬时外向钾电流（I to）。H/R组钠电流显著降低，而L型钙电流和瞬时外向钾电流显著增加（均p<0.01）。TMCC（200和400μM）通过抑制稳态失活来预防H/R诱导的异常钠电流。它还通过抑制稳态激活和促进稳态失活来对抗H/R诱导的异常L型钙电流。此外，它通过抑制稳态激活来减轻H/R诱导的异常瞬时外向钾电流。TMCC通过改变离子通道功能来预防大鼠心室肌细胞中H/R诱导的心律失常。
