Transmural ventricular distribution of coronary blood flow during coronary beta 2-adrenergic receptor activation in dogs.

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Abstract
Coronary vessels have .beta.2-adrenergic receptors, but their role in distributing flow across the ventricular wall independently of cardiac metabolic and mechanical factors that influence coronary resistance is unknown. The working heart of open-chest dogs was studied and blood flow was measured with radioactive microspheres in 4 layers across the left ventricular wall before and during .beta.2-receptor activation by intracoronary infusions of salbutamol or isoproterenol. Myocardial .beta.1 receptors were blocked with practolol, and aortic pressure, heart rate and myocardial O2 consumption were prevented from changing significantly. .beta.2 activation produced a progressively greater increase in flow from the subendocardium to the subepicardium with a decrease in the subendocardial:subepicardial (I:O) ratio from 1.40-1.00. Coronary resistance decreased progressively from the subendocardium to the subepicardium. To assess the influence on the above results of the transmural redistribution of flow that normally is developed by myocardial contraction in the working heart, similar experiments were conducted in the empty beating heart. A 2-step vasodilation with salbutamol decreased the I:O flow ratio from 1.76-1.40 and then to 1.27. Coronary resistance decreased from the subendocardium to the subepicardium during both steps of vasodilation. For comparable increments of flow, the decrease in the I:O flow ratio in the empty beating heart was smaller than that in the working heart. Apparently the activation of coronary .beta.2 receptors redistributes flow toward the subepicardium by producing a larger vasodilation in this region independently of the metabolic and mechanical influences of heat contraction on coronary resistance. This effect is enhanced in the intact heart by the transmural gradient of resistance to flow produced by cardiac contraction.