膜电位光学映射评估左室壁除颤过程中的虚拟电极

V. Fast, O. Sharifov, Eric R. Cheek, Jonathan C. Newton, R. Ideker
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引用次数: 62

摘要

背景:人们认为除颤是由于休克引起的大部分心室心肌跨膜电位(&Dgr;Vm)的变化(所谓的虚拟电极),但缺乏实验证据证明这一假设。本研究首次利用光学成像技术在左心室(LV)的分离制备中测量了内壁激波诱导的&Dgr;Vm。方法与结果:从猪心脏(n=9)中取出lv制剂,经冠状动脉灌注。在动作电位平台期间,通过两个大电极在壁上施加矩形冲击(持续时间10 ms,场强E≈2至50 V/cm)。使用16×16光电二极管阵列(分辨率1.2 mm/二极管)在跨壁壁面上测量冲击诱导的&Dgr;Vm。弱冲击(E≈2 V/cm)在壁中部产生可忽略的&Dgr;Vm,而强冲击在壁中部产生两种类型的&Dgr;Vm。(1) E>4 V/cm的冲击同时产生正、负的内部&Dgr;Vm,并随着冲击极性的改变而改变其符号,可能反映了组织结构的大规模不均匀性;&Dgr;Vm模式不对称,&Dgr;V−m>&Dgr;V+m。(2) E>34 V/cm的冲击在整个跨壁表面主要产生负的&Dgr;Vm,与冲击极性无关。这些相对均匀的极化可能是组织结构中微观不连续性的结果。结论:强除颤可诱发左室内层&Dgr;Vm。在动作电位平台期,内部的&Dgr;Vm通常是不对称的(&Dgr;V - m>&Dgr;V+m),并且在非常强的冲击期间变为全局负的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Intramural Virtual Electrodes During Defibrillation Shocks in Left Ventricular Wall Assessed by Optical Mapping of Membrane Potential
Background—It is believed that defibrillation is due to shock-induced changes of transmembrane potential (&Dgr;Vm) in the bulk of ventricular myocardium (so-called virtual electrodes), but experimental proof of this hypothesis is absent. Here, intramural shock-induced &Dgr;Vm were measured for the first time in isolated preparations of left ventricle (LV) by an optical mapping technique. Methods and Results—LV preparations were excised from porcine hearts (n=9) and perfused through a coronary artery. Rectangular shocks (duration 10 ms, field strength E ≈2 to 50 V/cm) were applied across the wall during the action potential plateau by 2 large electrodes. Shock-induced &Dgr;Vm were measured on the transmural wall surface with a 16×16 photodiode array (resolution 1.2 mm/diode). Whereas weak shocks (E≈2 V/cm) induced negligible &Dgr;Vm in the wall middle, stronger shocks produced intramural &Dgr;Vm of 2 types. (1) Shocks with E>4 V/cm produced both positive and negative intramural &Dgr;Vm that changed their sign on changing shock polarity, possibly reflecting large-scale nonuniformities in the tissue structure; the &Dgr;Vm patterns were asymmetrical, with &Dgr;V−m>&Dgr;V+m. (2) Shocks with E>34 V/cm produced predominantly negative &Dgr;Vm across the whole transmural surface, independent of the shock polarity. These relatively uniform polarizations could be a result of microscopic discontinuities in tissue structure. Conclusions—Strong defibrillation shocks induce &Dgr;Vm in the intramural layers of LV. During action potential plateau, intramural &Dgr;Vm are typically asymmetrical (&Dgr;V−m>&Dgr;V+m) and become globally negative during very strong shocks.
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