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与心室细胞耦合的异位灶实验模型。

Experimental model for an ectopic focus coupled to ventricular cells.

作者信息

Kumar R, Wilders R, Joyner R W, Jongsma H J, Verheijck E E, Golod D A, van Ginneken A C, Goolsby W N

机构信息

Todd Franklin Cardiac Research Laboratory, Department of Pediatrics, Emory University, Atlanta, Ga 30322, USA.

出版信息

Circulation. 1996 Aug 15;94(4):833-41. doi: 10.1161/01.cir.94.4.833.

DOI:10.1161/01.cir.94.4.833
PMID:8772708
Abstract

BACKGROUND

We used a mathematical model of a sinoatrial nodal cell (SAN model) electrically coupled to real ventricular cells (VCs) to investigate action potential conduction from an automatic focus.

METHODS AND RESULTS

Since input resistance of a VC is less than that of an SAN cell, coupling of the SAN model, with a size factor of 1, to a VC produced either (1) spontaneous pacing at the slower rate of the SAN model but without driving (activation) of the VC for lower values of coupling conductance (Gj) or (2) inhibition of pacing of the SAN model by electrical coupling to the VC for higher values of Gj. When the SAN model was adjusted in size to be 3 to 5 times larger than a sinoatrial nodal cell, thus making effective SAN model capacitance 3 to 5 times larger and input resistance 3 to 5 times smaller, the SAN model propagated activity to the coupled VC for Gj above a critical value. When the VC was paced at 1 Hz, the coupled cell pair demonstrated a stable rhythm of alternating cycle lengths and alternating conduction directions. By increasing pacing frequency to 2 Hz, we converted this rhythm to a regular 2-Hz frequency in which each action potential originated in the VC. More complex periodic interactions were observed at intermediate cycle lengths and lower or higher values of Gj.

CONCLUSIONS

The phenomena we observed demonstrate the critical role of the size of an automatic focus as well as the coupling in the propagation of activity from the focus into surrounding myocardium.

摘要

背景

我们使用了一个与真实心室细胞(VC)电耦合的窦房结细胞数学模型(SAN模型)来研究自搏性起搏点的动作电位传导。

方法与结果

由于VC的输入电阻小于SAN细胞的输入电阻,将大小因子为1的SAN模型与VC耦合,在较低耦合电导(Gj)值时会产生以下两种情况之一:(1)以SAN模型较慢的速率进行自发起搏,但不会驱动(激活)VC;或者(2)在较高Gj值时,通过与VC的电耦合抑制SAN模型的起搏。当将SAN模型的大小调整为比窦房结细胞大3至5倍时,从而使有效的SAN模型电容增大3至5倍,输入电阻减小3至5倍,对于高于临界值的Gj,SAN模型可将活动传播至耦合的VC。当以1Hz对VC进行起搏时,耦合的细胞对表现出周期长度交替和传导方向交替的稳定节律。通过将起搏频率增加到2Hz,我们将这种节律转换为规则的2Hz频率,其中每个动作电位都起源于VC。在中间周期长度以及较低或较高Gj值时观察到更复杂的周期性相互作用。

结论

我们观察到的现象证明了自搏性起搏点大小以及耦合在活动从起搏点向周围心肌传播中的关键作用。

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