Contributions of Purkinje-myocardial coupling to suppression and facilitation of early afterdepolarization-induced triggered activity.
Contributions of Purkinje-myocardial coupling to suppression and facilitation of early afterdepolarization-induced triggered activity.
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浦肯野心肌耦合对抑制和促进早期后除极诱导的触发活动的贡献。
DOI：
10.1109/tbme.2005.851528
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Pollard,AndrewE
中科院分区：
文献类型：
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作者：
Schafferhofer-Steltzer,Ingrid;Hofer,Ernst;Huelsing,DelilahJ;Bishop,SanfordP;Pollard,AndrewE
心室肌的电负荷调节浦肯野-心室连接处（PVJ）附近的传导系统复极。我们研究了负荷如何抑制和促进早期后除极（埃兹）的条件下，有一个高度的功能耦合的组织类型之间，这是一致的解剖安排在外周传导系统-心肌界面。实验在8只家兔右心室游离壁标本上完成。局部灌流自由运动的浦肯野束，记录束的动作电位。RV游离壁浸泡在正常溶液中。在股插入下游游离壁心肌附近记录表面电图。详细的组织学进行组装的计算机模型与散布浦肯野和心室肌细胞弱耦合整个区域。从浦肯野上行到下游外周传导系统和心肌激活的延迟在实验和模拟之间是相当的，支持模型节点到节点电耦合，即，功能耦合。实验中使用局部异丙肾上腺素延长浦肯野动作电位时程（APD）和模拟中使用钙电流增强均未能建立埃兹。延迟整流钾电流抑制或L型钙电流增强伴随浦肯野APD延长的模拟心肌APD延长，然而，EAD诱导的触发活动的发展。总的来说，我们的研究结果表明，当组织类型之间存在高度的功能耦合时，心肌下沉的竞争性贡献，从抑制到促进EAD诱导的触发活动的转变严重依赖于心肌APD延长。
Electrical loading by ventricular myocardium modulates conduction system repolarization near Purkinje-ventricular junctions (PVJs). We investigated how that loading suppresses and facilitates early afterdepolarizations (EADs) under conditions where there is a high degree of functional coupling between tissue types, which is consistent with the anatomic arrangement at the peripheral conduction system-myocardial interface. Experiments were completed in eight rabbit right ventricular (RV) free wall preparations. Free-running Purkinje strands were locally superfused, and action potentials were recorded from strands. RV free walls were bathed in normal solution. Surface electrograms were recorded near strand insertions into downstream free wall myocardium. Detailed histology was performed to assemble a computer model with interspersed Purkinje and ventricular myocytes weakly coupled throughout the region. Delays from Purkinje upstrokes to downstream peripheral conduction system and myocardial activation were comparable between experiments and simulations, supporting model node-to-node electrical coupling, i.e., the functional coupling. Purkinje action potential duration (APD) prolongation with localized isoproterenol in experiments and calcium current enhancement in simulations failed to establish EADs. With myocardial APD prolongation by delayed rectifier potassium current inhibition or L-type calcium current enhancement accompanying Purkinje APD prolongation in simulations, however, EAD-induced triggered activity developed. Collectively, our findings suggest competing contributions of the myocardial sink when there is a high degree of functional coupling between tissue types, with the transition from suppression to facilitation of EAD-induced triggered activity depending critically upon myocardial APD prolongation.