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A model of gap junction conductance and ventricular tachyarrhythmia

机译:间隙连接电导和室性心律失常的模型

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Cardiac gap junctions (GJs) form low resistance pathways along which the electrical impulse flows rapidly and repeatedly between all the cells of the myocardium, enabling coordinated contraction of the heart. In many heart diseases, electrical coupling through GJ channels between cardiomyocytes is down regulated. We set up a mathematical model of a chain of myocardial fibers to study how changing the coupling affects the activity of autorhythmic myocytes. While uncoupling blocked the propagation of excitation from autorhythmic myocytes to surrounding quiescent but excitable cells, different degrees of uncoupling increased the automaticity of the cells. Our modeling data suggests that the number of autorhythmic cells plays a key role in the excitation of autorhythmic cells and the conduction of impulses. We conclude that the degree of uncoupling between cardiomyocytes, induced by pathological processes, may generate ectopic foci, tachyarrhythmias being the outcome.
机译:心脏间隙连接(GJs)形成低电阻通路,电脉冲沿着该通路快速反复地在心肌的所有细胞之间流动,从而使心脏协调收缩。在许多心脏病中,通过心肌细胞之间的GJ通道进行的电耦合被下调。我们建立了一条心肌纤维链的数学模型,以研究改变耦合如何影响自律性心肌细胞的活性。尽管解偶联阻止了自律性肌细胞向周围静止但可兴奋的细胞的激发传播,但不同程度的解偶联增加了细胞的自动化程度。我们的建模数据表明,自律性细胞的数量在自律性细胞的激发和脉冲传导中起关键作用。我们得出的结论是,病理过程引起的心肌细胞之间的解偶联程度可能会产生异位灶,从而导致快速性心律失常。

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