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[急性缺血状态下心肌细胞电功能和机械功能紊乱的建模]

[Modeling of disturbances in electrical and mechanical function of cardiomyocytes under acute ischemia].

作者信息

Vikulova N A, Vasil'eva A D, Zamaraev D É, Solov'eva O É, Markhasin V S

出版信息

Biofizika. 2014 Sep-Oct;59(5):973-82.

PMID:25730982
Abstract

The effect of acute myocardial ischemia on the electrical and mechanical function of cardiomyocytes was studied in the framework of a mathematical model of a single cardiomyocyte. Acute ischemia consequences were simulated via a combination of two factors--a reduction of intracellular ATP concentration and an increase in extracellular potassium concentration, which affect the kinetics of ATP-sensitive potassium current and other potassium currents. In accord with experimental data, ischemic models produce action potential shortening and diastolic depolarization, which reduce contractile, ability of cardiomyocytes, Utilizing a 'difference-current integral' approach, we assessed quantitative contribution of ionic currents to changes in the action potential generation during ischemic injuries. It has been shown that an increase in the amplitude of inward rectifier potassium current I(K1) with increased extracellular potassium concentration has most essential contribution to the changes in the action potential duration under ischemia.

摘要

在单个心肌细胞数学模型的框架内,研究了急性心肌缺血对心肌细胞电功能和机械功能的影响。通过两个因素的组合来模拟急性缺血的后果——细胞内ATP浓度降低和细胞外钾浓度升高,这两个因素会影响ATP敏感性钾电流和其他钾电流的动力学。与实验数据一致,缺血模型会导致动作电位缩短和舒张期去极化,从而降低心肌细胞的收缩能力。利用“差分流积分”方法,我们评估了离子电流对缺血损伤期间动作电位产生变化的定量贡献。结果表明,随着细胞外钾浓度升高,内向整流钾电流I(K1)的幅度增加对缺血状态下动作电位持续时间的变化起了最重要的作用。

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