Argentieri T M, Frame L H, Colatsky T J
Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia.
Circ Res. 1990 Jan;66(1):123-34. doi: 10.1161/01.res.66.1.123.
The passive electrical properties of subendocardial Purkinje 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 fiber 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.
运用微电极技术和电缆理论，对冠状动脉结扎24小时后犬心室梗死区域内心内膜下浦肯野纤维的被动电特性进行了研究。在正常心脏中，发现心内膜下浦肯野纤维束内的细胞彼此之间耦合良好，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，得出的被动电特性估计值与先前对游离浦肯野纤维束的研究结果基本一致（膜长度常数，1.2±0.1毫米；膜时间常数，7.3±0.8毫秒；输入电阻，67.4±7.4千欧；膜电阻，8.2±0.7千欧·厘米；轴向电阻，0.52±0.06兆欧/厘米；膜电容，960±102纳法/厘米）（n = 21）。冠状动脉结扎后的当天，心内膜下浦肯野纤维动作电位延长且略有去极化。测量发现输入电阻（+40.5%）、膜电阻（+43.9%）和轴向电阻（+47.5%）显著增加，而膜电容显著降低（-24.3%）（n = 19）。传导速度以及动作电位波峰的膜长度常数、膜时间常数、时间常数和电容保持不变。这些结果与相邻细胞间的电脱耦一致，电脱耦会增加内部电阻率，同时伴随着细胞磷脂含量的变化，这会增加膜电阻并改变膜电容。或者，这些结果可以用一个简单模型来解释，即表观电结构仅通过电耦合的变化而改变，特定电特性保持不变。尽管观察到的变化背后的机制仍不确定，但本研究表明心肌梗死与存活的心内膜下浦肯野纤维的被动电结构改变有关，这与动作电位形态的变化一起，可能为冠状动脉结扎24小时后室性心律失常的发生提供了基础。
