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心脏中的机械电反馈:来自健康和患病组织的多细胞制剂及单细胞的细胞内微电极记录证据

Mechano-Electric Feedback in the Heart: Evidence from Intracellular Microelectrode Recordings on Multicellular Preparations and Single Cells from Healthy and Diseased Tissue

作者信息

Kamkin Andre, Kiseleva Irina, Wagner Kay-Dietrich, Scholz Holger

机构信息

Department of Fundamental and Applied Physiology, State Medical University of Russia, Ostrovitjanova Str. 1, 117997 Moscow, Russia

Institute of Physiology, Humboldt-University, Charité, Tucholskystrasse 2, 10117 Berlin, Germany

PMID:21290768
Abstract

We report on studies applying intracellular microelectrode recordings and whole-cell current measurements to investigate the effect of mechanical stretch on the electrical properties of cells from normal and diseased heart. Imposing physical stretch on atrial and ventricular tissue specimens elicited stretch-induced depolarizations (SID) of cardiomyocytes. Extra-action potentials occurred in the multicellular tissue preparations when the SIDs reached a threshold potential. Isolated cardiomyocytes responded to stretch with membrane depolarization, prolongation of their action potential (AP) and extra-APs that correlated with the amplitude of a non-selective stretch-activated current (I). At negative potentials, I was negative and carried by a transmembrane influx of Na ions, which induced diastolic depolarization or SID. Whilst the reaction of cardiomyocytes to mechanical stretch was independent of their spatial orientation (edgewise or broadwise), their response to compression was different and determined by the relative position of each cell. The sensitivity of the AP to mechanical stretch was significantly increased in hypertrophied myocardium, and this could be related to the expression of SACs.

摘要

我们报告了一些研究,这些研究应用细胞内微电极记录和全细胞电流测量来探究机械拉伸对正常和患病心脏细胞电特性的影响。对心房和心室组织标本施加物理拉伸会引发心肌细胞的拉伸诱导去极化(SID)。当SID达到阈电位时,多细胞组织制剂中会出现额外的动作电位。分离的心肌细胞对拉伸的反应是膜去极化、动作电位(AP)延长以及与非选择性拉伸激活电流(I)幅度相关的额外AP。在负电位时,I为负,由钠离子的跨膜内流携带,这会诱导舒张期去极化或SID。虽然心肌细胞对机械拉伸的反应与其空间取向(边缘或宽面)无关,但它们对压缩的反应不同,且由每个细胞的相对位置决定。肥厚心肌中AP对机械拉伸的敏感性显著增加,这可能与拉伸激活通道(SACs)的表达有关。

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