We tested the hypothesis that impaired coronary autoregulation, decreased flow reserve, and diminished reactive hyperemic response in hypertrophied hearts with coronary arterial hypertension may be reversible after relief of pressure overload. In 4-week ascending aortic banded rats, in vivo peak systolic left ventricular pressure increased to 178±8 mm Hg (103±6 mm Hg in sham-operated control group). This increased pressure produced myocardial hypertrophy, and the left ventricular weight/body weight ratio was 46% above that of the control group. After the rats were killed, the coronary perfusion pressure-flow relations were obtained during resting conditions and maximal vasodilation after a 40-second period of ischemia in beating but nonworidng isolated hearts perfused with Tyrode's solution with bovine red blood cells and albumin. In hearts from control rats, coronary autoregulation (i. I n normal hearts, coronary blood flow decreases only slightly with reduction of perfusion pressure in the autoregulatory range. 1 In the subendocardium of hypertrophied hearts with hypertension, autoregulation is impaired in the lower range of coronary perfusion pressure.2 Furthermore, coronary flow reserve estimated with adenosine, dipyridamole, or flow increases during stress or after ischemia is also decreased in hypertrophied hearts.3 -23 In previous studies, 24 -25 we reported that the maximal coronary flow rate during reactive hyperemia decreased in cardiac hypertrophy, but the decreased flow normalized after relief of pressure overload. Also, Anderson et al 26 reported that decreased flow reserve and coronary vascular structural changes in the spontaneously hypertensive rat were reversible after antihypertensive drug administration. However, there is no information concerning the reversibility of impaired coronary autoregulation in hypertrophied hearts. In the present study, we tested the hypothesis that the impaired coronary autoregulation and diminished hyperemic response to brief ischemia may reverse after relief of pressure overload. For this purpose, we used an experimental model consisting of ascending aortic banding and debanding in the rat. After isolation of the heart, we studied coronary hemodynamics in beating but nonworking hearts perfused with Tyrode's solution with bovine red blood cells and albumin because coronary autoregulation depends on myocardial metabolism.1 Moreover, because coronary flow reserve depends on coronary perfusion pressure, 118 we attempted to determine coronary flow reserve from coronary pressure-flow relations during resting conditions and during maximal vasodilation after brief ischemia.
MethodsWe used male Wistar rats 6-8 weeks old. After opening the chest, we banded the ascending aorta. Four weeks after banding, we operated on the rats again for the purpose of debanding some of them. We studied coronary hemodynamics in the following