Influence of Apamin on the Extracellularly Recorded Action Potentials Profiles of Subepicardial Cardiomyocytes of the Rat Heart in Myocardial Infarction

Pub Date : 2024-08-29 DOI:10.1134/s0022093024040057

A. V. Stepanov, M. G. Dobretsov, Yu. A. Filippov, I. V. Kubasov

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Abstract

The role of small-conductance Ca²⁺-activated K⁺-channels (SK channels) in the pathogenesis of cardiomyopathies of various etiologies remains poorly understood. The purpose of this work was to evaluate the effect of the blocker of SK channels, apamin, on the extracellularly recorded action potentials (eAPs) of subepicardial myocytes in the left ventricles of sham-operated rats and rats with myocardial infarction caused by ischemia-reperfusion. It was found that local delivery of the SK channel blocker apamin at a concentration of 500 nM to the eAP recording area did not affect the eAP profiles in the group of sham-operated rats but caused a significant slowdown in the repolarization time and a decrease in the afterhyperpolarization phase of eAPs in the group of rats with myocardial infarction. These data suggest that changes in the waveform of eAPs after infarction are associated with increased expression and/or activity of SK channels in subepicardial myocytes. The possible role of these channels in the structural and functional remodeling of the myocardium of the left ventricle of the heart after ischemia-reperfusion is discussed.

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阿帕明对心肌梗死大鼠心脏心外膜下心肌细胞胞外记录的动作电位曲线的影响

本研究的目的是评估SK通道阻断剂阿帕明对假手术大鼠和缺血再灌注心肌梗死大鼠左心室心外膜下心肌细胞动作电位（eAPs）的影响。研究发现，在eAP记录区域局部注射浓度为500 nM的SK通道阻滞剂阿帕明不会影响假手术大鼠组的eAP曲线，但会导致心肌梗死大鼠组eAP的复极时间显著减慢，超极化后阶段下降。这些数据表明，心肌梗死后 eAPs 波形的变化与心外膜下心肌细胞中 SK 通道的表达和/或活性增加有关。讨论了这些通道在缺血再灌注后左心室心肌的结构和功能重塑中的可能作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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