• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Ionic mechanisms of electrophysiological heterogeneity and conduction block in the infarct border zone.
【24h】

Ionic mechanisms of electrophysiological heterogeneity and conduction block in the infarct border zone.

机译：梗死边界区电生理异质性和传导阻滞的离子机制。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The increased incidence of arrhythmia in the healing phase after infarction has been linked to remodeling in the epicardial border zone (EBZ). Ionic models of normal zone (NZ) and EBZ myocytes were incorporated into one-dimensional models of propagation to gain mechanistic insights into how ion channel remodeling affects action potential (AP) duration (APD) and refractoriness, vulnerability to conduction block, and conduction safety postinfarction. We found that EBZ tissue exhibited abnormal APD restitution. The remodeled Na(+) current (I(Na)) and L-type Ca(2+) current (I(Ca,L)) promoted increased effective refractory period and prolonged APD at a short diastolic interval. While postrepolarization refractoriness due to remodeled EBZ I(Na) was the primary determinant of the vulnerable window for conduction block at the NZ-to-EBZ transition in response to premature S2 stimuli, altered EBZ restitution also promoted APD dispersion and increased the vulnerable window at fast S1 pacing rates. Abnormal EBZ APD restitution and refractoriness also led to abnormal periodic conduction block patterns for a range of fast S1 pacing rates. In addition, we found that I(Na) remodeling decreased conduction safety in the EBZ but that inward rectifier K(+) current remodeling partially offset this decrease. EBZ conduction was characterized by a weakened AP upstroke and short intercellular delays, which prevented I(Ca,L) and transient outward K(+) current remodeling from playing a role in EBZ conduction in uncoupled tissue. Simulations of a skeletal muscle Na(+) channel SkM1-I(Na) injection into the EBZ suggested that this recently proposed antiarrhythmic therapy has several desirable effects, including normalization of EBZ effective refractory period and APD restitution, elimination of vulnerability to conduction block, and normalization of conduction in tissue with reduced intercellular coupling.
机译：梗死后康复阶段心律失常的发生率增加与心外膜边界区（EBZ）的重塑有关。将正常区域（NZ）和EBZ心肌细胞的离子模型纳入一维传播模型中，从而获得有关离子通道重塑如何影响动作电位（AP）持续时间（APD）和耐火性，易受传导阻滞以及传导安全性的机制的见解梗死后。我们发现EBZ组织表现出异常的APD恢复。重塑的Na（+）电流（I（Na））和L型Ca（2+）电流（I（Ca，L））促进舒张期短时有效不应期延长和APD延长。虽然由于改建的EBZ I（Na）而导致的复极后耐火度是NZ-EBZ过渡对S2刺激做出反应时传导阻滞的脆弱窗口的主要决定因素，但改变的EBZ归还也促进了APD分散并增加了快速的S1起搏速度。 EBZ APD恢复和耐火度异常还导致一系列快速S1起搏率的周期性传导阻滞模式异常。此外，我们发现I（Na）重塑降低了EBZ的传导安全性，但向内整流器K（+）电流重塑部分抵消了这种下降。 EBZ传导的特点是减弱了AP上行冲程和较短的细胞间延迟，从而阻止了I（Ca，L）和瞬时向外K（+）电流重塑在未耦合组织中的EBZ传导中发挥作用。骨骼肌Na（+）通道SkM1-I（Na）注入EBZ的模拟表明，这种最近提出的抗心律不齐疗法具有多种理想的效果，包括EBZ有效不应期和APD恢复正常化，消除了对传导阻滞的脆弱性，和减少细胞间偶联的组织传导正常化。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号