Hysteresis and bistability in the direct transition from 1:1 to 2:1 rhythm in periodically driven single ventricular cells.

Hysteresis and bistability in the direct transition from 1:1 to 2:1 rhythm in periodically driven single ventricular cells.
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DOI:
10.1063/1.166465
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发表时间:
1999-12
期刊:
影响因子:
2.9
通讯作者:
A. Yehia;D. Jeandupeux;Francisco Alonso;M. Guevara
A. Yehia;D. Jeandupeux;Francisco Alonso;M. Guevara
中科院分区:
数学2区
文献类型:
--
作者:
A. Yehia;D. Jeandupeux;Francisco Alonso;M. Guevara

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本文报道了从家兔心室肌分离的单个静止细胞的跨膜电位。然后用通过相同的记录电极注入电池的周期性电流脉冲串驱动电池。当脉冲间隔或基本周期长度(BCL)足够长时,1:1节律产生,每个刺激脉冲产生动作电位。BCL的逐渐减少总是导致在某个点失去1:1同步。当脉冲幅度设置为固定的低水平并且BCL逐渐降低时,观察到N+1:N节律(N>/=2),使人联想到临床观察到的文氏节律。BCL进一步降低,然后产生2:1节律。相反,当脉冲幅度被设置为固定的高水平时,在2:1节律发生之前看到类似交替节律的周期加倍的2:2节律。在脉冲幅度被设置为中间电平(即,到文氏节律和交替节律之间的水平),随着BCL的降低,从1:1到2:1的节律直接转变:文氏节律和交替节律未被观察到。当此时BCL增加时,在比最初发生{1:1-->2:1}转变时的BCL更长的BCL处发生向1:1节律的转变,证明了滞后。随着BCL设置为滞后范围内的值,注射单个定时良好的额外刺激将1:1节律转换为2:1节律,反之亦然,提供了双稳态(在一组固定的刺激参数下两种不同的周期性节律共存)的无可争议的证据。当刺激幅度而不是BCL改变时,也可以看到1:1和2:1节律之间的滞后。使用数值积分的离子模型的一个单一的心室细胞制定为一个非线性系统的微分方程的模拟提供的结果是非常相似的实验中发现的。测定稳态动作电位持续时间恢复曲线,该曲线是1:1节律期间动作电位持续时间作为恢复时间或紧接在该动作电位之前的舒张间期的函数的图。在实验和建模工作中,使用恢复曲线推导的有限差分方程的迭代预测了直接{1:12:1}转变以及双稳态。然而,在2:1节律期间的动作电位时程的预测在实验中不如在模型中准确。最后,我们指出了我们的研究结果对心律失常的一些影响(例如,Mobitz II型阻滞,缺血性交替)。(c)1999年美国物理学会。
The transmembrane potential of a single quiescent cell isolated from rabbit ventricular muscle was recorded using a suction electrode in whole-cell recording mode. The cell was then driven with a periodic train of current pulses injected into the cell through the same recording electrode. When the interpulse interval or basic cycle length (BCL) was sufficiently long, 1:1 rhythm resulted, with each stimulus pulse producing an action potential. Gradual decrease in BCL invariably resulted in loss of 1:1 synchronization at some point. When the pulse amplitude was set to a fixed low level and BCL gradually decreased, N+1:N rhythms (N>/=2) reminiscent of clinically observed Wenckebach rhythms were seen. Further decrease in BCL then yielded a 2:1 rhythm. In contrast, when the pulse amplitude was set to a fixed high level, a period-doubled 2:2 rhythm resembling alternans rhythm was seen before a 2:1 rhythm occurred. With the pulse amplitude set to an intermediate level (i.e., to a level between those at which Wenckebach and alternans rhythms were seen), there was a direct transition from 1:1 to 2:1 rhythm as the BCL was decreased: Wenckebach and alternans rhythms were not seen. When at that point the BCL was increased, the transition back to 1:1 rhythm occurred at a longer BCL than that at which the {1:1-->2:1} transition had initially occurred, demonstrating hysteresis. With the BCL set to a value within the hysteresis range, injection of a single well-timed extrastimulus converted 1:1 rhythm into 2:1 rhythm or vice versa, providing incontrovertible evidence of bistability (the coexistence of two different periodic rhythms at a fixed set of stimulation parameters). Hysteresis between 1:1 and 2:1 rhythms was also seen when the stimulus amplitude, rather than the BCL, was changed. Simulations using numerical integration of an ionic model of a single ventricular cell formulated as a nonlinear system of differential equations provided results that were very similar to those found in the experiments. The steady-state action potential duration restitution curve, which is a plot of the duration of the action potential during 1:1 rhythm as a function of the recovery time or diastolic interval immediately preceding that action potential, was determined. Iteration of a finite-difference equation derived using the restitution curve predicted the direct {1:12:1} transition, as well as bistability, in both the experimental and modeling work. However, prediction of the action potential duration during 2:1 rhythm was not as accurate in the experiments as in the model. Finally, we point out a few implications of our findings for cardiac arrhythmias (e.g., Mobitz type II block, ischemic alternans). (c) 1999 American Institute of Physics.