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本文旨在分析酸中毒对心脏电生理活动的影响,探讨其诱发室性心律失常的机制.首先建立了具有pH和钙/钙调素依赖蛋白激酶Ⅱ(calcium/calmodulin dependent protein kinaseⅡ,Ca MKⅡ)调控作用的人体心室酸中毒计算模型,然后模拟了酸中毒过程中细胞和组织电活动的变化,并定量分析了心电图的改变情况.实验结果表明:在酸中毒期间,细胞动作电位时程的缩短和复极离散度的降低导致心电图QT间期缩短、T波幅值和宽度减小.同时,细胞静息电位的抬高和最大去极化速率的降低也促进了组织电兴奋的缓慢传导和传导阻滞.另外,酸中毒后的初期,肌浆网钙超载促进钙释放增多,导致细胞产生延迟后除极(delayed afterdepolarization,DADs),使心电图上表现为室性早搏.而缓慢传导、传导阻滞和室性早搏有利于折返波的产生,进而发展为室速.因此,酸中毒后细胞的触发活动是诱发室性心律失常的主要原因之一.
The purpose of this article is to analyze the effect of acidosis on cardiac electrophysiological activity and to explore the mechanism of ventricular arrhythmia induced by acidosis.Firstly, the mechanism of pH and calcium / calmodulin dependent protein kinase Ⅱ (Ca MKⅡ) And then simulate the change of cell and tissue electrical activity during acidosis and quantitatively analyze the changes of ECG.Experimental results show that during the period of acidosis, the shortening of cell action potential duration And the decrease of repolarization dispersion lead to shortening of QT interval and decrease of amplitude and width of T wave.At the same time, elevation of cell resting potential and decrease of maximum depolarization rate also promote the slow conduction of tissue electrical excitement and Conduction retardation.In addition, early after acidosis, calcium overload of sarcoplasmic reticulum increases the release of calcium, leading to delayed delayed dedelaction (DADs) of cells, which leads to premature ventricular contractions on ECG.The slow conduction and conduction Blocking and premature ventricular premature beats favor the generation of reentry waves, which in turn develop into ventricular tachycardia. Thus, the triggering activity of cells after acidosis is the induction of ventricular arrhythmias One of the main reasons.