Ursell P C, Gardner P I, Albala A, Fenoglio J J, Wit A L
Circ Res. 1985 Mar;56(3):436-51. doi: 10.1161/01.res.56.3.436.
Structural and electrophysiological properties of the epicardial muscle which survives on the surface of transmural infarcts of the canine heart (epicardial border zone) were studied at different times after occlusion of the left anterior coronary artery (LAD). Isolated preparations were superfused in vitro, transmembrane potentials recorded, and impulse propagation mapped. In preparations from subacute infarcts (1 and 5 days), resting potential, action potential amplitude, upstroke velocity, and duration were all significantly reduced. Well-defined directional differences in propagation occurred. Propagation was more rapid in the direction perpendicular to the left anterior coronary artery than in the direction perpendicular to the base of the heart, because of the uniform anisotropic structure of the surviving muscle fibers which were arranged in tightly packed bundles oriented perpendicular to the left anterior coronary artery. The only ultrastructural abnormalities found in these muscle fibers was an accumulation of large amounts of lipid droplets. As the infarcts healed, resting potential, action potential amplitude, and upstroke velocity returned to normal by 2 weeks, although action potential duration decreased further. Lipid droplets had disappeared, and connective tissue had invaded the epicardial border zone, separating the muscle bundles. By 2 months, action potentials were normal, but the muscle fibers were widely separated and disoriented by the connective tissue (parallel bundles no longer were found). In these regions with a nonuniform anisotropic structure, the well-defined directional differences in impulse propagation were lost. However, activation was very slow, perhaps because of diminished connections between cells. The persistence of slow conduction in healed infarcts may contribute to the occurrence of chronic arrhythmias.
在左冠状动脉前降支（LAD）闭塞后的不同时间，研究了存活于犬心透壁梗死表面（心外膜边缘区）的心外膜心肌的结构和电生理特性。将离体标本在体外进行灌流，记录跨膜电位，并绘制冲动传播图。在亚急性梗死（1天和5天）的标本中，静息电位、动作电位幅度、上升速度和时程均显著降低。冲动传播出现了明确的方向差异。由于存活的肌纤维呈均匀的各向异性结构，排列成紧密的束状，垂直于左冠状动脉前降支，因此在垂直于左冠状动脉前降支的方向上冲动传播比垂直于心底的方向更快。在这些肌纤维中发现的唯一超微结构异常是大量脂滴的积聚。随着梗死愈合，静息电位、动作电位幅度和上升速度在2周时恢复正常，尽管动作电位时程进一步缩短。脂滴消失，结缔组织侵入心外膜边缘区，使肌束分离。到2个月时，动作电位正常，但肌纤维被结缔组织广泛分离且排列紊乱（不再有平行束状结构）。在这些具有非均匀各向异性结构的区域，冲动传播中明确的方向差异消失。然而，激动非常缓慢，可能是因为细胞间连接减少。愈合梗死中缓慢传导的持续存在可能导致慢性心律失常的发生。
