Time course of infarct growth toward the endocardium after coronary occlusion.
Time course of infarct growth toward the endocardium after coronary occlusion.
复制标题
冠状动脉闭塞后梗塞向心内膜生长的时间过程。
DOI：
10.1152/ajpheart.1979.236.2.h356
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发表时间：
1979
期刊：
影响因子：
--
通讯作者：
A. L. Wit
中科院分区：
文献类型：
--
作者：
J. Fenoglio;H. Karagueuzian;P. Friedman;A. Albala;A. L. Wit
分别于冠脉结扎后1、3、5、6、14、24 h取材，观察心内膜下浦肯野纤维和心室肌纤维的跨膜电位和超微结构。随着梗死灶年龄的增加，动作电位从逐渐减少的肌细胞层记录下来。在14h时，几乎没有存活的肌肉。电生理活性肌纤维数量的减少与结构证据相关，即梗塞随着时间向心内膜表面移动，直到只剩下存活的浦肯野纤维。浦肯野和存活的心室肌纤维表现为静息电位、动作电位幅度和Vmax进行性降低，动作电位时程进行性延长。自发的舒张期去极化仅在24小时的心肌梗死中发现在浦肯野纤维中，偶尔在深至心内膜表面的细胞中被发现，这些细胞可能是肌肉细胞。我们假设在冠状动脉闭塞后的第一个24小时内，心律失常起源于梗死区和缺血区交界处附近。随着这个界面向心内膜移动，心律失常的起始点也随之移动，直到到达浦肯野网络。
Transmembrane potentials and ultrastructure of subendocardial Purkinje and ventricular muscle fibers, isolated 1, 3, 5, 6, 14, and 24 h after coronary occlusion were investigated. Action potentials were recorded from progressively fewer layers of muscle cells as the age of the infarct increased. At 14 h little viable muscle remained. The decrease in the number of electrophysiologically viable muscle fibers correlated with structural evidence that the infarct moved with time toward the endocardial surface until only viable Purkinje fibers remained. Purkinje and surviving ventricular muscle fibers demonstrated a progressive decrease in resting potential, action potential amplitude, and Vmax and a progressive increase in action potential duration. Spontaneous diastolic depolarizations were found in Purkinje fibers only in 24-h infarcts and occasionally in cells deep to the endocardial surface, which may have been muscle cells. We hypothesize that during the first 24 h after coronary occlusion arrhythmias originate near the interface of infarcted and ischemic myocardium. As this interface moves toward the endocardium, this site of origin of arrhythmias moves with it until the Purkinje network is reached.