Kalkman E A, van Haren P, Saxena P R, Schoemaker R G
Department of Pharmacology, Faculty of Medicine and Health Sciences, Erasmus University Rotterdam, The Netherlands.
J Mol Cell Cardiol. 1997 May;29(5):1487-97. doi: 10.1006/jmcc.1997.0388.
Remodelling after myocardial infarction (MI) is associated with vascular adaption, increasing vascular capacity of non-infarcted myocardium, and angiogenesis in the infarcted part during wound healing and scarring. We investigated regional vascular reactivity in the infarcted rat heart. Transmural infarction of the left ventricular free wall was induced by coronary artery ligation. After 3 weeks, regional flow during maximal vasodilation (nitroprusside, NPR) and submaximal vasoconstriction (arginine-vasopressin, AVP) were studied in buffer-perfused hearts. The main findings were: (1) a reduced vasodilator response (NPR) in the viable part of the left ventricular free wall, where hypertrophy was most pronounced, resulting in reduced maximal tissue perfusion of the myocardium bordering the scar (19.7 + 0.6 v 25.7 + 1.2 ml/min.g), whereas perfusion of other non-infarcted regions was preserved. (2) A 54% lower vasodilator response (NPR) and a 25% stronger vasoconstriction (AVP) in scar tissue compared to viable parts of MI hearts. Microscopy showed thicker walls of resistance arteries in scar tissue than in viable parts of MI hearts or in sham hearts, morphometrically substantiated by two- to three-fold greater wall/lumen ratios. These data indicate a deviant response of scar vessels of MI hearts, and in the non-infarcted part, a reduced coronary reserve in the most hypertrophied region. Whereas the former may be caused by different vessel structure, the reduced vasodilator reserve of the spared part of the left ventricular free wall may indicate vasodilation at rest due to insufficient vascular growth. Thus, the most hypertrophied region would be at the highest risk of further ischemic damage.
心肌梗死（MI）后的重塑与血管适应、非梗死心肌血管容量增加以及伤口愈合和瘢痕形成过程中梗死部位的血管生成有关。我们研究了梗死大鼠心脏的局部血管反应性。通过冠状动脉结扎诱导左心室游离壁透壁梗死。3周后，在缓冲液灌注的心脏中研究最大血管舒张（硝普钠，NPR）和次最大血管收缩（精氨酸加压素，AVP）期间的局部血流。主要发现如下：（1）左心室游离壁存活部分的血管舒张反应（NPR）降低，此处肥厚最为明显，导致瘢痕周围心肌的最大组织灌注减少（19.7 + 0.6对25.7 + 1.2 ml/min.g），而其他非梗死区域的灌注得以保留。（2）与MI心脏的存活部分相比，瘢痕组织中的血管舒张反应（NPR）降低54%，血管收缩（AVP）增强25%。显微镜检查显示，瘢痕组织中阻力动脉壁比MI心脏存活部分或假手术心脏中的厚，形态计量学证实壁/腔比值大两到三倍。这些数据表明MI心脏瘢痕血管的反应异常，在非梗死部分，最肥厚区域的冠状动脉储备减少。前者可能由不同的血管结构引起，而左心室游离壁 spared部分血管舒张储备降低可能表明由于血管生长不足导致静息时血管舒张。因此，最肥厚的区域将面临进一步缺血损伤的最高风险。
