Nonischemic myocardial damage induced by nonocclusive constriction of coronary artery in rats.
Nonischemic myocardial damage induced by nonocclusive constriction of coronary artery in rats.
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大鼠冠状动脉非闭塞性收缩引起的非缺血性心肌损伤。
DOI：
10.1152/ajpheart.1991.260.3.h651
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Anversa,P
中科院分区：
文献类型：
--
作者：
Capasso,JM;Li,P;Anversa,P
为了确定冠状动脉血管直径的减小是否导致心脏功能、冠状动脉灌注和组织完整性的改变，使大鼠的左冠状动脉变窄，并在手术后3天和5天测量心室血流动力学。冠状动脉平均狭窄62%，舒张末期压升高，而收缩压峰值、压力随时间的正变化、每搏输出量和总外周阻力降低。然而，这种功能损害伴随着静息冠状动脉血流量（CBF）的保存，尽管检测到最大CBF下降了43%。修复性纤维化和肌细胞溶解性坏死灶主要见于肌内膜和中层心肌。这些病变在时间上是不同的，分别对应于5天和12至24小时的心肌损伤形式。最大CBF的变化与狭窄程度相关，而体积分数、平均横截面积和每单位面积心肌修复性纤维化病变的病灶数仅与舒张末期压相关。总之，不影响静息冠状动脉灌注的主要冠状动脉的管腔直径的减小对心脏性能具有深远的不利影响，并引发正在进行的即刻肌细胞损失。因此，组织和细胞损伤本质上可能不是缺血性的，而是由其他机制介导的，例如无法承受的机械应力。
To determine whether reduction in coronary vessel diameter leads to alterations in cardiac function, coronary perfusion, and tissue integrity, the left coronary artery of rats was narrowed and ventricular hemodynamics measured at 3 and 5 days after surgery. Coronary artery narrowing averaged 62% and end-diastolic pressure was increased, whereas peak systolic pressure, positive change in pressure over time, stroke volume, and total peripheral resistance were decreased. However, this impairment of function was accompanied by a preservation of resting coronary blood flow (CBF), although a 43% decrease in maximal CBF was detected. Foci of reparative fibrosis and myocytolytic necrosis were found primarily in the endomyocardium and midmyocardium. These lesions were temporally distinct, corresponding to 5 days and 12- to 24-h-old forms of myocardial damage, respectively. The changes in maximal CBF correlated with the degree of stenosis, whereas the volume fraction, average cross-sectional area, and number of foci of reparative fibrosis lesions per unit area of myocardium correlated exclusively with end-diastolic pressure. In conclusion, reductions in luminal diameter of a major coronary artery not affecting resting coronary perfusion have a profound detrimental impact on cardiac performance and initiate immediate myocyte cell loss that is ongoing. Thus tissue and cellular damage may not be ischemic in nature but rather mediated by other mechanisms such as unbearable mechanical stress.