Arrhythmogenic mechanism of gap junctional uncoupling

用光标测法研究了家兔心脏细胞间电解偶联的致心律失常机制。心肌缝隙连接的药理学抑制稳定了螺旋波折返的动力学，并促进其永久化，而增强缝隙连接耦合不稳定的螺旋波折返，并促进其早期自我终止，通过妥协的激励波的传播与强大的曲率附近的旋转中心。这些结果表明，加强缝隙连接偶联可能是一个有用的策略，用于治疗危及生命的心律失常的病变心脏缝隙连接重塑。

Arrhythmogenic mechanisms of intercellular electrical uncoupling was investigated by optical mapping of purfued rabbit hearts. Pharmacological inhibition of myocardial gap junctions stabilized the dynamics of spiral-wave reentry and facilitated its perpetuation, whereas enhancement of gap junctional coupling destabilized spiral-wave reentry and promoted its early self-termination by compromising propagation of excitation waves with strong curvature near the rotation center. These results suggest that enhancement of gap junctional coupling could be a useful strategy for the treatment of life-threatening arrhythmias in diseased hearts with gap junctional remodeling.