Billette J, Métayer R, St-Vincent M
Department of Physiology, Faculty of Medicine, University of Montreal, Quebec, Canada.
Circ Res. 1988 Apr;62(4):790-9. doi: 10.1161/01.res.62.4.790.
The slowly developing rate-induced prolongation in atrioventricular nodal conduction time, termed "fatigue," was selectively studied using specifically designed stimulation protocols in isolated rabbit heart preparations. A nodal recovery curve (A2H2 versus H1A2 intervals; nodal conduction time of each premature beat plotted against corresponding recovery time) was obtained before and after a stable and nearly maximum fatigue had been reached by driving the atrium for 5 minutes at a fast rate close to the upper limit of 1:1 nodal conduction. The fatigue uniformly prolonged all A2H2 intervals (12.3 +/- 1.3 msec) and systematically increased the minimum H1A2 interval at which complete nodal block occurred (24.8 +/- 4.0 msec) (p less than 0.01, n = 6). To study the rate and time dependence of fatigue, nodal conduction times were obtained during three rapid 5-minute pacings corresponding to 50%, 75%, and 100% shortening of the pacing interval in the 1:1 nodal conduction range. The respective maximum fatigue-induced increases in conduction time were 5.4 +/- 1.8, 9.0 +/- 2.7, and 12.5 +/- 2.1 msec (p less than 0.01, n = 6). However, the pacing interval had no significant effect on the time required to reach either 50% (17.1 +/- 3.5 seconds) or 90% (92.6 +/- 15.4 seconds) of the fatigue observed after 5 minutes of fast rate. At the termination of any rapid stimulation, the fatigue effect dissipated with a time course that was inverse but symmetrical to that of its induction. These findings support the existence of an independent, slow, nodal memory process by which the conduction time changes according to past events with a long time constant.
使用专门设计的刺激方案,在离体兔心脏标本中选择性地研究了房室结传导时间中缓慢发展的速率诱导延长现象,即“疲劳”。在以接近1:1房室结传导上限的快速频率驱动心房5分钟,达到稳定且接近最大疲劳状态之前和之后,获得了一个结恢复曲线(A2H2与H1A2间期;每个早搏的结传导时间与相应的恢复时间作图)。疲劳使所有A2H2间期均一性延长(12.3±1.3毫秒),并系统性地增加了发生完全性结阻滞时的最小H1A2间期(24.8±4.0毫秒)(p<0.01,n = 6)。为了研究疲劳的速率和时间依赖性,在对应于1:1结传导范围内起搏间期缩短50%、75%和100%的三次快速5分钟起搏过程中,获得了结传导时间。疲劳诱导的传导时间最大增加量分别为5.4±1.8、9.0±2.7和12.5±2.1毫秒(p<0.01,n = 6)。然而,起搏间期对达到快速频率5分钟后观察到的疲劳的50%(17.1±3.5秒)或90%(92.6±15.4秒)所需的时间没有显著影响。在任何快速刺激终止时,疲劳效应以与其诱导过程相反但对称的时间进程消散。这些发现支持了一种独立、缓慢的结记忆过程的存在,通过该过程,传导时间根据过去的事件以较长的时间常数发生变化。