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一种通过二维心脏合胞体进行传播的大规模并行计算机模型。

A massively parallel computer model of propagation through a two-dimensional cardiac syncytium.

作者信息

Fishler M G, Thakor N V

机构信息

Johns Hopkins University School of Medicine, Baltimore, Maryland.

出版信息

Pacing Clin Electrophysiol. 1991 Nov;14(11 Pt 2):1694-9. doi: 10.1111/j.1540-8159.1991.tb02750.x.

DOI:10.1111/j.1540-8159.1991.tb02750.x
PMID:1721160
Abstract

A computer model of electrical propagation through a two-dimensional (2D) sheet of cardiac tissue has been developed to run on the massively parallel processor Connection Machine (CM-2) computer. The transmembrane ionic currents in each of 16,384 (128 x 128) 100 x 100 microns 2 patches of cardiac tissue are described by modified Beeler-Reuter membrane equations. These equations, along with the parabolic differential equation derived from 2D cable theory, are solved in parallel to study normal and abnormal 2D propagation. The sheet is paced with planar waves at a basic cycle length of 500 msec (control). When a premature ectopic stimulus of sufficient strength and appropriate timing is then applied to a local region of the syncytium, one of two types of reentry is observed: (a) stable figure-of-eight reentry, or (b) unstable but self-sustaining "fibrillation-like" reentry. During this fibrillatory activity, action potential durations are 79.8 +/- 36.8 msec (control = 244.9 +/- 0.9 msec) and coupling intervals average 96.7 +/- 31.3 msec (control = 500 +/- 0 msec). We also observed that passive electrotonically-induced depolarization of already refractory tissue extended the refractory period of that tissue, and that the duration of this extension depended on the magnitude of the electrotonic effect.

摘要

已开发出一种通过二维(2D)心脏组织片进行电传播的计算机模型,以便在大规模并行处理器连接机(CM - 2)计算机上运行。16384个(128×128)100×100微米²的心脏组织片块中的每一个的跨膜离子电流,都由修正的比勒 - 罗伊特膜方程描述。这些方程与从二维电缆理论推导出来的抛物型微分方程一起并行求解,以研究正常和异常的二维传播。该片块以基本周期长度为500毫秒(对照)的平面波进行起搏。当随后向合胞体的局部区域施加具有足够强度和适当时间的过早异位刺激时,会观察到两种类型的折返之一:(a)稳定的8字形折返,或(b)不稳定但自我维持的“颤动样”折返。在这种颤动活动期间,动作电位持续时间为79.8±36.8毫秒(对照 = 244.9±0.9毫秒),耦合间期平均为96.7±31.3毫秒(对照 = 500±0毫秒)。我们还观察到,已经处于不应期的组织的被动电紧张诱导的去极化延长了该组织的不应期,并且这种延长的持续时间取决于电紧张效应的大小。

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