心脏电生理变化和下调的连接蛋白43提示离体大鼠心脏低温缺血再灌注损伤引起的再灌注心律失常

贵州医科大学     麻醉与心脏电生理课题组

翻译：陈锐  编辑：陈锐  审核：曹莹

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摘要：本研究的目的是确定单相动作电位 (MAP) 变化作为低温缺血再灌注心律失常生物标志物的效用。对低温缺血再灌注模型进行60分钟的心脏停搏，而将离体的大鼠心脏用大量4°C冷KH溶液保存。在再灌注期间，监测心脏的心律失常和单相动作电位。使用HE和TTC染色评估心肌损伤。免疫组织化学和蛋白质印迹用于评估连接蛋白43 (Cx43)和Akt的表达和分布。总之，动作电位持续时间延长，复极化分散度增加，下调和偏侧化的Cx43都导致了心脏电传导的紊乱，这可能是心脏停搏后低温缺血性心脏心律失常发生的基础。MAP可用作低温缺血再灌注引起的心律失常的生物标志物。

关键词： 心脏骤停；心麻痹; 连接蛋白 43; 低温再灌注心律失常; 单相动作电位。

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原始文献来源： 

Jing Yi , Hongwei Duan , Kaiyuan Chen , et al. Cardiac Electrophysiological Changes and Downregulated Connexin 43 Prompts Reperfusion Arrhythmias Induced by Hypothermic Ischemia-Reperfusion Injury in Isolated Rat Hearts

.[J].Journal of Cardiovascular Translational Research , 2022 June 10, DOI: 10.1007/s12265-022-10256-7.

英文原文

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Downregulated Connexin 43 Prompts Reperfusion Arrhythmias Induced by Hypothermic Ischemia-Reperfusion Injury in Isolated Rat Hearts

Abstract

The purpose of this study was to determine the utility of the monophasic action potential (MAP) changes as an arrhythmic biomarker in hypothermic ischemia-reperfusion. The hypothermic ischemia-reperfusion model was subjected to 60 min of cardioplegic arrest while the isolated rat hearts were preserved with a multidose cold K-H solution at 4 °C. During the reperfusion period, the heart's arrhythmia and monophasic action potential were also monitored. The myocardial damage was assessed using HE and TTC stains. Immunohistochemistry and Western blotting were used to assess the expression and distribution of Connexin 43 (Cx43) and Akt. Collectively, prolonged action potential durations, increased dispersion of repolarization, and downregulated and lateralized Cx43 all contribute to the derangement of electrical impulse propagation that may underlie arrhythmogenesis in the cold ischemic heart following cardioplegic arrest. MAP might be used as a biomarker for arrhythmias caused by hypothermic ischemia-reperfusion.

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