Spontaneous activity induced in rabbit Purkinje myocytes during coupling to a depolarized model cell.
Spontaneous activity induced in rabbit Purkinje myocytes during coupling to a depolarized model cell.
复制标题
在与去极化模型细胞耦合期间诱导兔浦肯野肌细胞的自发活动。
DOI：
10.1016/s0008-6363(03)00507-8
复制
发表时间：
2003
影响因子：
10.8
通讯作者：
Pollard,AndrewE
中科院分区：
文献类型：
--
作者：
Huelsing,DelilahJ;Spitzer,KennethW;Pollard,AndrewE
目的：“损伤电流”的发展继发于非均质离子积累和细胞在缺血边界区解耦已被认为是急性缺血期间引起心律失常的触发因素。本研究的目的是确定损伤电流通过浦肯野-心室界面对异常自动性发展的影响。方法：采用膜片钳和电子细胞偶联技术记录兔浦肯野肌细胞的动作电位，并对其施加损伤电流。损伤电流取决于：(1)耦合电阻的变化，以模拟不同程度的细胞解耦；(2)浦肯野膜电位和去极化缺血心肌的差异，由初始电压为−70、−60或−50 mV的无源电阻-电容电路表示。结果：在偶联到中度去极化细胞（−60或−50 mV）期间，浦肯野肌细胞在偶联阻力窗口内发生重复的自发活动。这种异常的自动性依赖于l型钙电流，因为镉或硝苯地平完全抑制了偶联诱导的自发活性。结论：我们的研究结果表明，损伤电流可以诱导正常浦肯野肌细胞的自发活动。心肌去极化水平和诱导这种活动所需的细胞解偶联程度表明，损伤电流诱导的自发性浦肯野活动是急性缺血性心律失常的有力触发因素。
Objective: The development of an “injury current” secondary to heterogeneous ion accumulation and cellular uncoupling across the ischemic border zone has been implicated as a trigger for arrhythmias arising during acute ischemia. The purpose of the present study was to determine the effects of injury current across the Purkinje–ventricular interface in the development of abnormal automaticity.Methods:Patch clamp and electronic cell coupling techniques were used to record action potentials from and to apply injury current to isolated rabbit Purkinje myocytes. Injury current was dependent upon: (1) a coupling resistance, which was varied to simulate different degrees of cellular uncoupling, and (2) the difference in Purkinje membrane potential and depolarized ischemic myocardium, which was represented by a passive resistor–capacitor circuit with initial voltages of −70, −60, or −50 mV.Results:During coupling to the moderately depolarized cell (−60 or −50 mV), Purkinje myocytes developed repetitive, spontaneous activity within a window of coupling resistances. This abnormal automaticity was dependent upon L-type calcium current, as cadmium or nifedipine completely suppressed coupling-induced spontaneous activity.Conclusions:Our results demonstrate that injury current alone can induce spontaneous activity in normal Purkinje myocytes. The level of myocardial depolarization and the degree of cellular uncoupling required to induce this activity suggest spontaneous Purkinje activity induced by injury current as a potent trigger for acute ischemic arrhythmias.