ELECTRICAL-PROPERTIES OF CANINE SUBENDOCARDIAL PURKINJE-FIBERS SURVIVING IN 1-DAY-OLD EXPERIMENTAL MYOCARDIAL-INFARCTION
ELECTRICAL-PROPERTIES OF CANINE SUBENDOCARDIAL PURKINJE-FIBERS SURVIVING IN 1-DAY-OLD EXPERIMENTAL MYOCARDIAL-INFARCTION
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DOI：
10.1161/01.res.66.1.123
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发表时间：
1990-01-01
影响因子：
20.1
通讯作者：
COLATSKY, TJ
中科院分区：
文献类型：
--
作者：
ARGENTIERI, TM;FRAME, LH;COLATSKY, TJ
本文应用微电极技术和电缆理论研究了结扎冠状动脉后24小时存活于犬心室梗塞区的内膜下Purikinje纤维的被动电特性。在正常心脏中，发现心内膜下浦肯野纤维束内的细胞彼此耦合良好，但与相邻心肌电隔离。对细胞内电流注入的电压响应与一维电缆行为一致，并产生了与先前对自由运行的浦肯野链的工作（膜长度常数，1.2 ± 0.001）大体一致的被动电特性的估计。0.1膜时间常数为7.3 ± 0.01mm。0.8，毫秒;输入电阻，67.4 ±。7.4 K Ω;膜电阻，8.2 ±。0.7 K.OMEGA. cm;轴向阻力，0.52 ±. 0.06 M.OMEGA./ cm;膜电容，960. ±. 102 nF/cm）（n=21）。冠脉结扎后第二天，内膜下浦肯野纤维动作电位延长，并轻度去极化。测量到输入电阻（+40.5%）、膜电阻（+43.9%）和轴向电阻（+47.5%）显著增加，而发现膜电容显著降低（-24.3%）（n=19）。传导速度、膜长度常数、膜时间常数、以及用于足的动作电位的时间常数和电容均保持不变。这些结果与相邻细胞之间的电解偶联一致，这将增加内部电阻率，伴随着细胞磷脂含量的变化，这可以增加膜电阻并改变膜电容。或者，可以用一个简单的模型来解释结果，在这个模型中，表观电结构仅由电耦合的变化来改变，而特定的电特性保持不变。虽然所观察到的变化的机制仍然不确定，本研究表明，心肌梗死是与存活subendocellular浦肯野纤维的被动电结构的改变，其中，连同动作电位配置的变化，可能提供一个基板的生成室性心律失常冠状动脉结扎后24小时。
The passive electrical properties of subendocardial Purikinje fibers surviving in infarcted regions of canine ventricle 24 hours after coronary ligation were studied by using microelectrode techniques and cable theory. In normal hearts, cells within the subendocardial Purkinje fibers strands were found to be well coupled to each other but electrically isolated from neighboring myocardium. Voltage response to intracellular current injection was consistent with one-dimensional cable behavior and yielded estimates of passive electrical properties in general agreement with previous work on free-running Purkinje strands (membrane length constant, 1.2.+-.0.1 mm; membrane time constant, 7.3.+-.0.8, msec; input resistance, 67.4.+-.7.4 K.OMEGA.; membrane resistance, 8.2.+-.0.7 K.OMEGA. cm; axial resistance, 0.52.+-.0.06 M.OMEGA./cm; membrane capacitance, 960.+-.102 nF/cm) (n=21). On the day after coronary ligation, subendocardial Purkinje fiber action potentials were prolonged and slightly depolarized. Significant increases were measured in input resistance (+40.5%), membrane resistance (+43.9%), and axial resistance (+47.5%), whereas membrane capacitance was found to be significantly decreased (-24.3%) (n=19). Conduction velocity, membrane length constant, membrane time constant, and the time constant and capacitance for the foot of the action potential remained unchanged. These results are consistent with electrical uncoupling between adjacent cells, which will increase internal resistivity, accompanied by changes in cellular phospholipid content, which can increase membrane resistance and alter membrane capacitance. Alternatively, the results can be explained by a simple model in which the apparent electrical structure is altered by changes in electrical coupling alone, with specific electrical properties remaining constant. Although the mechanisms underlying the observed changes remain uncertain, the present study indicates that myocardial infarction is associated with alterations in the passive electrical structure of surviving subendocardial Purkinje fibers, which, together with changes in action potential configuration, may provide a substrate for the generation of ventricular arrhythmias 24 hours after coronary ligation.