Regionally different vascular response to vasoactive substances in the remodelled infarcted rat heart; aberrant vasculature in the infarct scar.

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.