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心脏组织中折返的诱发。缺失的环节:电场如何改变跨膜电位。

The induction of reentry in cardiac tissue. The missing link: How electric fields alter transmembrane potential.

作者信息

Roth Bradley J., Krassowska Wanda

机构信息

Department of Physics and Astronomy, Vanderbilt University, Nashville, Tennessee 37235.

出版信息

Chaos. 1998 Mar;8(1):204-220. doi: 10.1063/1.166298.

Abstract

This review examines the initiation of reentry in cardiac muscle by strong electric shocks. Specifically, it concentrates on the mechanisms by which electric shocks change the transmembrane potential of the cardiac membrane and create the physiological substrate required by the critical point theory for the initiation of rotors. The mechanisms examined include (1) direct polarization of the tissue by the stimulating current, as described by the one-dimensional cable model and its two- and three-dimensional extensions, (2) the presence of virtual anodes and cathodes, as described by the bidomain model with unequal anisotropy ratios of the intra- and extracellular spaces, (3) polarization of the tissue due to changing orientation of cardiac fibers, and (4) polarization of individual cells or groups of cells by the electric field ("sawtooth potential"). The importance of these mechanisms in the initiation of reentry is examined in two case studies: the induction of rotors using successive stimulation with a unipolar electrode, and the induction of rotors using cross-field stimulation. These cases reveal that the mechanism by which a unipolar stimulation induces arrhythmias can be explained in the framework of the bidomain model with unequal anisotropy ratios. In contrast, none of the examined mechanisms provide an adequate explanation for the induction of rotors by cross-field stimulation. Hence, this study emphasizes the need for further experimental and theoretical work directed toward explaining the mechanism of field stimulation. (c) 1998 American Institute of Physics.

摘要

本综述探讨强电击引发心肌折返的机制。具体而言,它聚焦于电击改变心肌细胞膜跨膜电位并创造临界点理论启动转子所需生理底物的机制。所探讨的机制包括:(1)如一维电缆模型及其二维和三维扩展所描述的,刺激电流对组织的直接极化;(2)如细胞内和细胞外空间各向异性比率不等的双域模型所描述的虚拟阳极和阴极的存在;(3)由于心肌纤维取向变化导致的组织极化;以及(4)电场对单个细胞或细胞群的极化(“锯齿状电位”)。在两个案例研究中考察了这些机制在折返启动中的重要性:使用单极电极连续刺激诱导转子,以及使用交叉场刺激诱导转子。这些案例表明,单极刺激诱发心律失常的机制可以在各向异性比率不等的双域模型框架内得到解释。相比之下,所考察的机制均无法充分解释交叉场刺激诱导转子的现象。因此,本研究强调需要开展进一步的实验和理论工作来解释场刺激的机制。(c)1998美国物理研究所。

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