Mitochondrial depolarization and electrophysiological changes during ischemia in the rabbit and human heart.

Mitochondrial depolarization and electrophysiological changes during ischemia in the rabbit and human heart.
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兔子和人心脏缺血期间的线粒体去极化和电生理变化。

DOI:
10.1152/ajpheart.00437.2014
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发表时间:
2014
期刊:
American journal of physiology. Heart and circulatory physiology
影响因子:
--
通讯作者:
Efimov,IgorR
Efimov,IgorR
中科院分区:
--
文献类型:
--
作者:
Sulkin,MatthewS;Boukens,BasJ;Tetlow,Megan;Gutbrod,SarahR;Ng,FuSiong;Efimov,IgorR

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Instability of the inner mitochondrial membrane potential (ΔΨm) has been implicated in electrical dysfunction, including arrhythmogenesis during ischemia-reperfusion. Monitoring ΔΨmhas led to conflicting results, where depolarization has been reported as sporadic and as a propagating wave. The present study was designed to resolve the aforementioned difference and determine the unknown relationship between ΔΨmand electrophysiology. We developed a novel imaging modality for simultaneous optical mapping of ΔΨmand transmembrane potential (Vm). Optical mapping was performed using potentiometric dyes on preparations from 4 mouse hearts, 14 rabbit hearts, and 7 human hearts. Our data showed that during ischemia, ΔΨmdepolarization is sporadic and changes asynchronously with electrophysiological changes. Spatially, ΔΨmdepolarization was associated with action potential duration shortening but not conduction slowing. Analysis of focal activity indicated that ΔΨmis not different within the myocardium where the focus originates compared with normal ventricular tissue. Overall, our data suggest that during ischemia, mitochondria maintain their function at the expense of sarcolemmal electrophysiology, but ΔΨmdepolarization does not have a direct association to ischemia-induced arrhythmias.
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