Li Z Y, Wang Y H, Maldonado C, Kupersmith J
Department of Medicine, Michigan State University, East Lansing 48824.
Cardiovasc Res. 1994 Aug;28(8):1277-84. doi: 10.1093/cvr/28.8.1277.
The aim was to examine under abnormal conditions the flow of currents across junctional (J-) cells found between Purkinje fibre cells and ventricular muscle cells, and determine whether these currents play a role in increasing the excitation rate of ventricular muscle.
Canine Purkinje fibre and papillary muscle preparations were mapped to locate the Purkinje fibre-ventricular muscle cell junction (PVJ). Using standard techniques, action potentials from Purkinje fibres, J-cells, and ventricular muscle cells and extracellular electrograms were simultaneously recorded at the PVJ. The tissue was then superfused with Tyrode solution plus 4.5-5.0 mmol of ethylenediamine tetra-acetate (EDTA).
EDTA prolonged the action potential duration mainly in Purkinje fibres. Secondary plateaus were recorded at membrane potentials of -63.5(SD 7.6) mV (n = 16) in J-cells, and at membrane potentials of -74.9(4.3) mV (n = 9) in ventricular muscle cells. Triggered activations appeared on both secondary plateaus with the earliest site of activation at J-cells (n = 12), at ventricular muscle cells (n = 4), or in both (n = 6). Tetrodotoxin (3-9 x 10(-7) M) and verapamil (1 x 10(-6)-10(-5) M) suppressed triggered activations.
The PVJ zone appears to be an important site for the generation of triggered activations. Interventions suggest that triggered activations originating in the J-cell depend on delayed repolarisations which trigger the activation of sodium and/or calcium channels.
本研究旨在检测在异常情况下,浦肯野纤维细胞与心室肌细胞之间的连接(J-)细胞上电流的流动情况,并确定这些电流是否在提高心室肌兴奋速率中发挥作用。
绘制犬浦肯野纤维和乳头肌标本图,以定位浦肯野纤维-心室肌细胞连接点(PVJ)。采用标准技术,在PVJ处同时记录浦肯野纤维、J-细胞和心室肌细胞的动作电位以及细胞外电图。然后用含4.5 - 5.0 mmol乙二胺四乙酸(EDTA)的Tyrode溶液对组织进行灌流。
EDTA主要延长了浦肯野纤维的动作电位时程。在J-细胞中,膜电位为-63.5(标准差7.6)mV(n = 16)时记录到次级平台,在心室肌细胞中,膜电位为-74.9(4.3)mV(n = 9)时记录到次级平台。在两个次级平台上均出现触发激活,最早激活部位在J-细胞(n = 12)、心室肌细胞(n = 4)或两者均有(n = 6)。河豚毒素(3 - 9×10⁻⁷ M)和维拉帕米(1×10⁻⁶ - 10⁻⁵ M)可抑制触发激活。
PVJ区似乎是触发激活产生的重要部位。干预措施表明,起源于J-细胞的触发激活依赖于延迟复极化,后者触发钠通道和/或钙通道的激活。