Cardiac Cellular Coupling and the Spread of Early Instabilities in Intracellular Ca2+
Cardiac Cellular Coupling and the Spread of Early Instabilities in Intracellular Ca2+
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DOI：
10.1016/j.bpj.2012.02.034
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发表时间：
2012-03-21
影响因子：
3.4
通讯作者：
Entcheva, Emilia
中科院分区：
文献类型：
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作者：
Jia, Zhiheng;Bien, Harold;Entcheva, Emilia
最近的实验和建模研究表明，精细的空间尺度，复杂的性质，和独立的贡献的Ca2+动力学作为一个programmic因素在心脏。细胞水平的Ca2+不稳定性（称为交替）进展为组织水平心律失常的机制尚不清楚。由于间隙连接耦合决定心脏合胞体的属性，我们着手阐明其在时空演变的Ca2+不稳定性的作用。我们在体外实验干扰心脏合胞体细胞偶联。耦合定量荧光恢复光漂白后，和相关的功能，包括微妙的精细尺度的Ca2+交替，捕获的光学映射。交替的传导速度和阈值随着耦合的增加而单调增加。低耦合增强了Ca 2+交替幅度，但早期的空间扩展（
Recent experimental and modeling studies demonstrate the fine spatial scale, complex nature, and independent contribution of Ca2+ dynamics as a proarrhythmic factor in the heart. The mechanism of progression of cell-level Ca2+ instabilities, known as alternans, to tissue-level arrhythmias is not well understood. Because gap junction coupling dictates cardiac syncytial properties, we set out to elucidate its role in the spatiotemporal evolution of Ca2+ instabilities. We experimentally perturbed cellular coupling in cardiac syncytium in vitro. Coupling was quantified by fluorescence recovery after photobleaching, and related to function, including subtle fine-scale Ca2+ alternans, captured by optical mapping. Conduction velocity and threshold for alternans monotonically increased with coupling. Lower coupling enhanced Ca2+ alternans amplitude, but the spatial spread of early (