CO, Pb ++ and SO2 effects on L-type calcium channel and action potential in human atrial myocytes. In silico study

TecnoLogicas Pub Date : 2017-09-04 DOI:10.22430/22565337.718
Diana C. Pachajoa, C. Tobón, J. P. Ugarte, J. Saiz
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引用次数: 1

Abstract

Exposure to air pollutants like carbon monoxide (CO), lead (Pb++) and sulfur dioxide (SO2) promotes the occurrence of cardiovascular diseases. Experimental studies have shown that CO, Pb++ and SO2 block L-type calcium channels, reducing the calcium current (ICaL) and the action potential duration (APD), which favors the initiation of atrial arrhythmias. The goal is to study the effects of CO, Pb++ and SO2 at different concentrations on ICaL and action potential using computational simulation. For this purpose, models of the effects of the air pollutants on the atrial L-type calcium channel were developed and were incorporated into a mathematical model of a human atrial cell. The results suggest that CO, Pb++ and SO2 block the ICaL current in a fraction that increases along with the concentration, generating an APD shortening. These results are consistent with experimental studies. The combined effect of the three air pollutants produced an APD shortening, which is considered to be a pro-arrhythmic effect.
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CO、Pb++和SO2对人心房肌细胞L型钙通道和动作电位的影响。计算机研究
暴露于一氧化碳(CO)、铅(Pb++)和二氧化硫(SO2)等空气污染物会促进心血管疾病的发生。实验研究表明,CO、Pb++和SO2阻断L型钙通道,降低钙电流(ICaL)和动作电位持续时间(APD),有利于房性心律失常的发生。目的是通过计算模拟研究不同浓度的CO、Pb++和SO2对ICaL和作用电位的影响。为此,开发了空气污染物对心房L型钙通道影响的模型,并将其纳入人类心房细胞的数学模型中。结果表明,CO、Pb++和SO2以随浓度增加的分数阻断ICaL电流,产生APD缩短。这些结果与实验研究一致。三种空气污染物的联合作用导致APD缩短,这被认为是一种促心律失常的作用。
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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发文量
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审稿时长
28 weeks
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