Reduced regional myocardial perfusion in the presence of pharmacologic vasodilator reserve

To determine whether reductions in regional myocardial perfusion at reduced coronary arterial pressures reliably indicate maximal vasodilation of the distal vasculature, coronary autoregulation was studied in open-chest dogs at heart rates of ~60 beats/min, a level at which metabolic demand, time-average systolic compressive forces, and transmural vasodilator reserve approximate those found under usual resting conditions. Circumflex pressure was controlled with a programmable pressure source. Regional circumflex inflow was 0.56 ± 0.04(SEM) ml·min^-1·g^-1 when circumflex pressure equaled spontaneous aortic pressure and fell to 0.34 ± 0.02 ml·min^-1·g^-1 when circumflex pressure was reduced to 35 mm Hg. Reductions were similar in each myocardial layer, with endocardial flow falling from 0.68 ± 0.04 to 0.39 ± 0.03 ml·min^-1·g^-1. During adenosine-induced vasodilation at 35 mm Hg, full-thickness and endocardial flows rose to 0.92 ± 0.08 and 1.07 ± 0.10 ml·min^-1·g^-1, respectively. When coronary pressure was reduced to 25 mm Hg and autoregulation was againg operative, full-thickness and endocardial flows fell to 0.28 ± 0.03 and 0.28 ± 0.04 ml·min^-1·g^-1. During adenosine vasodilation at 25 mm Hg endocardial flow did not increase significantly but epicardial reserve remained present. These results indicate that significant reductions in regional myocardial perfusion can occur before pharmacologic vasodilator reserve is exhausted. In the absence of tachycardia, endocardial vasodilator reserve can persist to coronary pressures less than 35 mm Hg, but is ordinarily exhausted before epicardial vasodilator reserve.