Cardiac pacemaker cell failure with preserved I(f), I(CaL), and I(Kr): a lesson about pacemaker function learned from ischemia-induced bradycardia.
Cardiac pacemaker cell failure with preserved I(f), I(CaL), and I(Kr): a lesson about pacemaker function learned from ischemia-induced bradycardia.
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DOI：
10.1016/j.yjmcc.2006.11.009
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发表时间：
2007-02
影响因子：
5
通讯作者：
V. Maltsev;E. Lakatta
中科院分区：
文献类型：
--
作者：
V. Maltsev;E. Lakatta
心肌缺血是一个重要的全球性健康问题。它会导致收缩失败、心律失常和心脏细胞死亡。窦性心动过缓的特征是缓慢的心率（< 60 bpm），这是一种明显的缺血相关心律失常，直接由心脏初级起搏细胞（SANC）衰竭导致的窦房结（SAN）内心跳启动不足引起。Yi-Mei Du和Richard Nathan在本期《分子和细胞心脏病学杂志》[1]上发表的研究涉及孤立SANC中缺血诱导心动过缓的离子基础。他们的研究结果不仅有助于理解缺血引起的心动过缓，而且有助于阐明心脏起搏细胞功能的基本机制。
Cardiac ischemia is an important global health problem. It leads to contraction failure, arrhythmias, and cardiac cell death. Sinus bradycardia characterized by a slow heart rate (< 60 bpm) is a prominent ischemia-related arrhythmia directly caused by a deficiency of heart beat initiation within the sinoatrial node (SAN), due to a failure of the heart’s primary pacemaker cells (SANC). The study presented by Yi-Mei Du and Richard Nathan in this issue of Journal of Molecular and Cellular Cardiology [1] deals with the ionic basis of ischemia-induced bradycardia in isolated SANC. The results of their study not only contribute to understanding of ischemia-induced bradycardia, but also help to delineate the fundamental mechanisms of cardiac pacemaker cell function.