SIDE-TO-SIDE SLIPPAGE OF MYOCYTES PARTICIPATES IN VENTRICULAR WALL REMODELING ACUTELY AFTER MYOCARDIAL-INFARCTION IN RATS
SIDE-TO-SIDE SLIPPAGE OF MYOCYTES PARTICIPATES IN VENTRICULAR WALL REMODELING ACUTELY AFTER MYOCARDIAL-INFARCTION IN RATS
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DOI：
10.1161/01.res.67.1.23
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发表时间：
1990-07-01
影响因子：
20.1
通讯作者：
ANVERSA, P
中科院分区：
文献类型：
--
作者：
OLIVETTI, G;CAPASSO, JM;ANVERSA, P
为了确定与心肌梗死相关的急性左心衰竭是否会导致保留的非缺血部分的室壁结构改变，在大鼠身上制造了大面积的梗塞，并在术后2天处死动物。左心室舒张末压升高，左心室dp/dt和收缩压降低，提示存在严重的心功能不全。心肌梗死的绝对面积，通过测量左心室游离壁肌细胞核丢失的比例来确定，平均为63%。中腔横向直径增加了20%，壁厚减少了33%。心肌细胞壁数减少36%，毛细血管轮廓减少40%。这些功能异常和室壁结构重排的结合导致舒张期室壁应力增加7.8倍。一项对室间隔的对比分析显示，间隔厚度上的细胞数量减少了24%，而毛细血管减少了26%。此外，计算出这一脑室区域的舒张期应力增加了7.2倍。舒张期应力的增加分别与室壁和隔膜中22%和16%的心肌细胞肥大有关。综上所述，心肌细胞的侧向滑移与大面积心肌梗死后的心室扩张有关，并有助于心室重构和失代偿性离心性肥厚的发生。
To determine whether acute left ventricular failure associated with myocardial infarction leads to architectural changes in the spared nonischemic portion of the ventricular wall, large infarcts were produced in rats, and the animals were killed 2 days after surgery. Left ventricular end-diastolic pressure was increased, whereas left ventricular dP/dt and systolic pressure were decreased, indicating the presence of severe ventricular dysfunction. Absolute infarct size, determined by measuring the fraction of myocyte nuclei lost from the left ventricular free wall, averaged 63%. Transverse midchamber diameter increased by 20%, and wall thickness diminished by 33%. The mural number of myocytes in this spared region of the left ventricular free wall decreased by 36% and the capillary profiles by 40%. The combination of these functional abnormalities and structural rearrangement of the wall resulted in a 7.8-fold increase in diastolic wall stress. A comparable analysis of the interventricular septum demonstrated a 24% reduction in the number of cells across the septal thickness, whereas capillaries were diminished by 26%. Moreover, a 7.2-fold elevation in diastolic stress was computed in this region of the ventricle. The augmentation in diastolic stress was associated with a 22% and a 16% myocyte cellular hypertrophy in the wall and septum, respectively. In conclusion, side-to-side slippage of myocytes in the myocardium occurs in association with ventricular dilatation after a large myocardial infarction and contributes to ventricular remodeling and the occurrence of decompensated eccentric hypertrophy.