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Block of impulse propagation at an abrupt tissue expansion: evaluation of the critical strand diameter in 2- and 3-dimensional computer models

机译:突发组织扩张时脉冲传播的阻滞:在2维和3维计算机模型中评估临界股线直径

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Objective: Unidirectional conduction block in the heart can occur at a site where the impulse is transmitted from a small to a large tissue volume. The aim of this study was to evaluate the occurrence of conduction block in a 2-dimensional and 3-dimensional computer model of cardiac tissue consisting of a narrow strand abruptly emerging into a large area. In this structure, the strand diameter critical for the occurrence of block, hc, was evaluated as a function of changes in the active and passive electrical properties of both the strand and the large medium. Methods: The effects of changes in the following parameters on hc were analysed: (1) maximum sodium conductance (gNamax), (2) longitudinal (Rx) and transverse (Ry) intracellular resistivities, and (3) inhomogeneities in gNamax and Rx and Ry between the strand and the large area. Three ionic models for cardiac excitation described by Beeler-Reuter, Ebihara-Johnson, and Luo-Rudy ionic current kinetics were compared. Results: In the 2-dimensional simulations, hc was 175 μm in Ebihara-Johnson and Beeler-Reuter models and 200 μm in the Luo-Rudy model. At the critical strand diameter, the site of conduction block was located beyond the transition, i.e. a small circular area was activated in the large medium, whereas with narrower strands conduction block occurred within the strands. The decrease of gNamax resulted in a large increase of hc. This increase was mainly due to the change of gNamax in the large area, while hc was almost independent of gNamax in the strand. Changing Rx had no effect on hc, whereas the increase of Ry decreased hc and reversed conduction block. Inhomogeneous changes of Rx and Ry in the strand versus the large medium had opposite effects on hc. When the resistivities of the strand alone were increased, hc also increased. In contrast, the increase of the resistivities in the large area reduced hc. In the 3-dimensional model, hc was 2.7 times larger than the corresponding 2-dimensional values at the various levels of gNamax and resistivity. Conclusions: (1) At physiological values for active and passive electrical properties, hc in the 2D simulations is close to 200 μm in all three ionic models. In the 3-dimensional simulations, hc is 2.7 larger than in the 2-dimensional models. (2) The excitable properties of the large area but not of the strand modify hc. The decrease of intercellular coupling in the large medium facilitates impulse conduction and reduces hc, while the same change in the strand increases hc. (3) Occurrence of conduction block at an abrupt geometrical transition can be explained by both the impedance mismatch at the transition site and the critical curvature beyond the transition
机译:目的:心脏中的单向传导阻滞可能发生在冲动从小到大的组织体积传递的部位。这项研究的目的是评估心脏组织的二维和三维计算机模型中的传导阻滞的发生,该模型由突然出现的大区域的窄链组成。在这种结构中,对于发生块的临界线直径hc被评估为线和大介质的有源和无源电性能变化的函数。方法:分析以下参数变化对hc的影响:(1)最大钠电导(gNamax),(2)纵向(Rx)和横向(Ry)细胞内电阻率,以及(3)gNamax和Rx的不均匀性以及在钢绞线和大面积区域之间的Ry。比较了Beeler-Reuter,Ebihara-Johnson和Luo-Rudy的离子电流动力学描述的三种用于心脏兴奋的离子模型。结果:在二维模拟中,Ebihara-Johnson和Beeler-Reuter模型的hc为175μm,而Luo-Rudy模型的hc为200μm。在临界股线直径处,传导阻滞的位置位于过渡区之外,即,在大的介质中激活了一个小的圆形区域,而在股线较窄的情况下,传导阻滞发生在股线内。 gNamax的减少导致hc大量增加。这种增加主要是由于大面积gNamax的变化,而hc几乎与链中的gNamax无关。改变Rx对hc没有影响,而Ry的增加会降低hc并逆转传导阻滞。与大型培养基相比,链中Rx和Ry的不均匀变化对hc具有相反的影响。当单线的电阻率增加时,hc也增加。相反,在大面积内电阻率的增加降低了hc。在3维模型中,在不同的gNamax和电阻率水平下,hc比相应的2维值大2.7倍。结论:(1)在有源和无源电特性的生理值下,二维模拟中的hc在所有三个离子模型中均接近200μm。在3维仿真中,hc比2维模型大2.7。 (2)大面积的兴奋性而不是链的兴奋性改变了hc。大培养基中细胞间偶联的减少促进了脉冲传导并降低了hc,而链中的相同变化增加了hc。 (3)在突然的几何过渡处发生传导阻滞可以用过渡处的阻抗失配和过渡后的临界曲率来解释

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