Whitney R T, Rozanski G J
Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68198-4575.
Am J Physiol. 1993 Oct;265(4 Pt 2):H1195-202. doi: 10.1152/ajpheart.1993.265.4.H1195.
A computer algorithm is described that used experimental data to model the arrhythmogenic interaction of phasic vagal stimuli and atrial ectopic pacemakers. The model consisted of a dominant sinus node and a single ectopic pacemaker center separated by conducting atrial tissue. Its primary operation was to predict the timing and incidence of atrial premature beats resulting from transient escape of ectopic automatic impulses when vagal-induced entrance block of the sinus impulse was simulated near the ectopic focus. These predictions were based on a series of experimentally derived phase-response and corrected recovery time curves, describing the modulation of ectopic pacemaker periodicity by vagal input and overdrive suppression, respectively. Depending on the combination of curves tested, the model predicted premature beats to develop only with critically timed vagal stimuli. The coupling intervals of vagal-induced premature beats were > 300 ms and varied as a function of vagal timing and sinus cycle length. The model suggests therefore that phasic vagal stimuli within the atrium may transiently protect ectopic pacemaker foci from conducted sinus impulses and mediate the genesis of atrial extrasystoles with long coupling intervals.
本文描述了一种计算机算法，该算法利用实验数据对阶段性迷走神经刺激与房性异位起搏器的致心律失常相互作用进行建模。该模型由一个占主导地位的窦房结和一个由传导性心房组织分隔的单个异位起搏点中心组成。其主要操作是预测当在异位起搏点附近模拟迷走神经诱导的窦房结冲动传入阻滞时，异位自动冲动短暂逸出导致房性早搏的时间和发生率。这些预测基于一系列实验得出的相位响应曲线和校正恢复时间曲线，分别描述了迷走神经输入和超速抑制对异位起搏器周期的调制。根据所测试曲线的组合，该模型预测只有在严格定时的迷走神经刺激下才会出现早搏。迷走神经诱导的早搏的耦合间期>300毫秒，并随迷走神经定时和窦性周期长度而变化。因此，该模型表明心房内的阶段性迷走神经刺激可能会暂时保护异位起搏点免受传导的窦房结冲动影响，并介导长耦合间期房性期前收缩的发生。
