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首页> 外文期刊>Cellular Physiology and Biochemistry >L-type calcium current (I_(Ca,L)) and inward rectifier potassium current (I_(K1)) are involved in QT prolongation induced by arsenic trioxide in rat
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L-type calcium current (I_(Ca,L)) and inward rectifier potassium current (I_(K1)) are involved in QT prolongation induced by arsenic trioxide in rat

机译：L型钙电流（I_（Ca，L））和内向整流钾电流（I_（K1））与三氧化二砷诱导的大鼠QT延长有关

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The present study was designed to study the effects of As_2O _3 on QT interval prolongation and to explore the potential ionic mechanisms in isolated rat ventricular cardiomyocytes. The rats of As _2O_3 group were treated with 0.8 mg·kg ~(-1)·d~(-1) As_2O_3 intravenously for 7 days consecutively and the control group with saline. The ECG was recorded to calculate heart rate-corrected QT interval (QTc). Single cardiomyocytes were isolated by using collagenase II, and the action potential duration (APD) and ion currents were recorded by whole-cell patch clamp. [Ca~(2+)] i was examined by confocal laser scanning microscopy. Our data showed that both QTc and APD were prolonged significantly after As_2O _3treatment. Meanwhile, As_2O_3 suppressed I _(K1) and shifted the reversal potential to more positive direction. Moreover, the density of I _(Ca,L) was augmented significantly, and the steady-state activation curve became more negative, whereas, the inactivation and reactivation of I _(Ca,L) were not changed notably after As _2O_3 administration. Furthermore, the maximal [Ca ~(2+)] _i was enhanced obviously by either KCl or caffeine stimulation in As_2O_3-treated cardiomyocytes. Our results show that the potential mechanism of As_2O_3-induced QT interval prolongation in rat might be relative to disturbing the fine balance of transmembrane currents (increasing I _(Ca,L) and decreasing I _(K1)) and causing APD prolongation.
机译：本研究旨在研究As_2O _3对QT间期延长的影响，并探讨离体大鼠心室心肌细胞的潜在离子机制。 As _2O_3组大鼠静脉内连续静脉注射0.8 mg·kg〜（-1）·d〜（-1）As_2O_3，对照组连续7天。记录心电图以计算经心率校正的QT间隔（QTc）。使用胶原酶II分离单个心肌细胞，并通过全细胞膜片钳记录动作电位持续时间（APD）和离子电流。用共聚焦激光扫描显微镜检查了[Ca〜（2 +）] i。我们的数据显示，As_2O _3处理后，QTc和APD均显着延长。同时，As_2O_3抑制了I _（K1）并将反向电位移向更正的方向。此外，I _（Ca，L）的密度显着增加，稳态活化曲线变得更负，而As _2O_3施用后I _（Ca，L）的失活和再活化没有明显变化。此外，在As_2O_3处理的心肌细胞中，通过KCl或咖啡因刺激，最大[Ca〜（2+）] _i明显增加。我们的结果表明，As_2O_3诱导大鼠QT间隔延长的潜在机制可能与干扰跨膜电流的精细平衡（增加I _（Ca，L）和降低I _（K1））并导致APD延长有关。

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