Arrhythmogenic mechanism of gap junctional uncoupling

利用光学成像技术对纯化兔心脏细胞间电解偶联的致心律失常机制进行了研究。心肌间隙连接的药物抑制稳定了螺旋波再入的动力学并促进了其延续，而间隙连接耦合的增强破坏了螺旋波再入的稳定性，并通过影响旋转中心附近具有强曲率的激发波的传播促进了螺旋波再入的早期自终止。这些结果表明，加强间隙连接耦合可能是治疗具有间隙连接重构的患病心脏中危及生命的心律失常的有效策略。

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.