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为了探讨细胞外低钾时引起长QT综合征单向传导阻滞的易损窗增大的原因,我们以改良的LR91一维非均质心室肌组织数学模型为研究对象,定量化研究了Na+通道电导及门控因子空间梯度的变化。同时,还观察了细胞外正常钾浓度和低钾对动作电位时程及各种离子通道电流的影响。实验分为正常组和LQTS组。分别以500、1 000和2 000 ms的刺激周长(BCL)对一维模型施加基础刺激S1(-70μA/μF、1.5 ms)。每10次S1后施加期前刺激S2,S1S2间期以1 ms的步长递减以测量易损窗。结果发现,细胞外低钾、长QT综合征及心率减慢是通过增大失活因子h*j空间分布梯度使GNa空间梯度增大的。结果还显示,细胞外低钾使IK、IK1电流峰值降低,这使LR91一维模型上心肌细胞AP复极延迟并且复极离散度增大。这可能是导致h*j和GNa空间梯度增大的重要原因之一。这些变化使产生单向传导阻滞的易损窗增大并增加室性心律失常的发生。
In order to investigate the reason why the vulnerable window of unidirectional block caused by long QT syndrome is caused by extracellular hypokalemia, we take the modified LR91 one-dimensional inhomogeneous ventricular muscle tissue model as the research object and quantitatively study the Na + Channel conductance and gating factor spatial gradient changes. At the same time, we also observed the extracellular normal potassium concentration and potassium on the action potential duration and various ion channel currents. The experiment was divided into normal group and LQTS group. The basal stimulus S1 (-70 μA / μF, 1.5 ms) was applied to the one-dimensional model with stimulation circumference (BCL) of 500, 1000 and 2000 ms, respectively. S2 was stimulated 10 times before the post-S1 administration period, and the S1S2 interval was decremented in steps of 1 ms to measure the vulnerable window. The results showed that extracellular hypokalemia, long QT syndrome and slow heart rate increase GNa spatial gradient by increasing the spatial distribution gradient of inactivating factor h * j. The results also show that extracellular hypokalemia IK, IK1 current peak decreased, which makes LR91 one-dimensional model of AP myocardial cell repolarization delay and repolarization dispersion increased. This may be one of the important reasons leading to the increase of h * j and GNa spatial gradients. These changes increase the vulnerable window with unidirectional block and increase the occurrence of ventricular arrhythmias.