Zhang H, Zhang Z X, Yang L, Jin Y B, Huang Y Z
The Key Laboratory of Biomedical Information Engineering of the Ministry of Education of China, Institute of Biomedical Engineering, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, PR China.
Gen Physiol Biophys. 2005 Dec;24(4):365-80.
A computer simulation method was used to study the possible role of electrical dispersion induced by regional ischemia in the mechanisms underlying cardiac arrhythmias. Ischemic cells were simulated by considering the three major component conditions of acute ischemia (elevated extracellular K+ concentration, acidosis and anoxia) at the level of ionic currents and ionic concentrations. An ischemic area was introduced into a homogeneous healthy tissue to create a localized inhomogeneity. The constructed models were solved using the operator splitting and adaptive time step methods. The numerical experiments showed that action potential durations (APDs) of ischemic cells did not change with beats of shorter or longer cycle length. The smaller percentage increase of slow component of the delayed rectifier K+ current, I(ks), and smaller outward Na+-Ca2+ exchange current were found to be the ionic mechanisms underlying the decreased rate dependence in ischemic cells. The results suggest that ischemia flattens the APD restitution curve; however, the dispersion of refractory period can be greatly increased by a premature beat in the constructed inhomogeneous sheet. This demonstrates that the dispersion of refractoriness rather than APD by a premature beat contributes to reentrant tachyarrhythmias in the locally ischemic tissue.
采用计算机模拟方法研究局部缺血诱发的电离散在心律失常发生机制中的可能作用。通过在离子电流和离子浓度水平上考虑急性缺血的三个主要组成条件（细胞外钾离子浓度升高、酸中毒和缺氧）来模拟缺血细胞。将缺血区域引入均匀的健康组织中以产生局部不均匀性。使用算子分裂和自适应时间步长方法求解构建的模型。数值实验表明，缺血细胞的动作电位时程（APD）不会随周期长度较短或较长的搏动而改变。延迟整流钾电流I(ks)的慢成分增加百分比更小，外向钠钙交换电流更小，被认为是缺血细胞中率依赖性降低的离子机制。结果表明，缺血使APD恢复曲线变平；然而，在构建的不均匀薄片中，早搏可使不应期离散度大大增加。这表明，早搏导致的不应期离散而非APD离散促成了局部缺血组织中的折返性快速心律失常。
