IKs protects from ventricular arrhythmia during cardiac ischemia and reperfusion in rabbits by preserving the repolarization reserve.
IKs protects from ventricular arrhythmia during cardiac ischemia and reperfusion in rabbits by preserving the repolarization reserve.
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DOI：
10.1371/journal.pone.0031545
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Wang S
中科院分区：
文献类型：
--
作者：
Guo X;Gao X;Wang Y;Peng L;Zhu Y;Wang S
复极储备在心肌缺血/再灌注期间预防室性心律失常中的作用以及缺血对缓慢激活的延迟整流钾电流（IKs）通道亚单位表达的影响尚不清楚。在兔冠状动脉左回旋支闭塞/再灌注模型上，观察了L-768，673阻断IKs（有或无缺血/再灌注）后，单相动作电位时程（MAPD）延长和三角测量的反应。缺血/再灌注和IKs阻断可显著诱导MAPD 90延长，并在再灌注后45 min、60 min和75 min增加心外膜区的三角测量，同时伴有同期室性早搏（PVBs）的增加。此外，在短暂性缺血或永久性梗死后检查IKs通道亚单位表达，并使用短暂性或慢性心脏缺血的兔模型评价β-肾上腺素能刺激激发的单相动作电位（MAP）波形的变化。在肾上腺素能刺激下，梗塞2天的心脏梗塞周围区的心外膜MAP表现出三角形增加。IKs通道的α亚基KCNQ 1蛋白在同一组中下调。这两个结果均与PVB发生率增加一致。阻断IKs导致MAP三角测量，从而诱发室性心律失常。慢性缺血增加肾上腺素能刺激下室性心律失常的发生率，并与梗死周围区MAP三角测量增加有关。KCNQ 1蛋白表达下调可能是这些变化的根本原因。
The function of the repolarization reserve in the prevention of ventricular arrhythmias during cardiac ischemia/reperfusion and the impact of ischemia on slowly activated delayed rectifier potassium current (IKs) channel subunit expression are not well understood. The responses of monophasic action potential duration (MAPD) prolongation and triangulation were investigated following an L-768,673-induced blockade of IKs with or without ischemia/reperfusion in a rabbit model of left circumflex coronary artery occlusion/reperfusion. Ischemia/reperfusion and IKs blockade were found to significantly induce MAPD90 prolongation and increase triangulation at the epicardial zone at 45 min, 60 min, and 75 min after reperfusion, accompanied with an increase in premature ventricular beats (PVBs) during the same period. Additionally, IKs channel subunit expression was examined following transient ischemia or permanent infarction and changes in monophasic action potential (MAP) waveforms challenged by β-adrenergic stimulation were evaluated using a rabbit model of transient or chronic cardiac ischemia. The epicardial MAP in the peri-infarct zone of hearts subjected to infarction for 2 days exhibited increased triangulation under adrenergic stimulation. KCNQ1 protein, the α subunit of the IKs channel, was downregulated in the same group. Both findings were consistent with an increased incidence of PVBs. Blockade of IKs caused MAP triangulation, which precipitated ventricular arrhythmias. Chronic ischemia increased the incidence of ventricular arrhythmias under adrenergic stimulation and was associated with increased MAP triangulation of the peri-infarct zone. Downregulation of KCNQ1 protein may be the underlying cause of these changes.
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影响因子：
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作者：
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