Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation.

The role of a-receptor constriction of coronary vessels in response to cardiac sympathetic activation was evaluated in closed-chest, chloralose-anesthetized dogs. Cardiac sympathetic activation was produced (1) directly by intracoronary norepinephrine infusion at several different rates and (2) reflexly by carotid sinus hypotension. The resulting changes in coronary blood flow and myocardial oxygen consumption were recorded before and after a-receptor blockade with dibozane (3.0 mg/kg, iv) or phenoxybenzamine (0.5 mg/kg, intracoronary). The changes in coronary blood flow were normalized to changes in myocardial metabolism by division of the oxygen delivery (coronary flow times arterial oxygen content) by the change in myocardial oxygen consumption per 100 g of myocardium. Before a-receptor blockade, either intracoronary norepinephrine infusion or reflex sympathetic activation from the carotid sinus resulted in an increase of only 0.85 ml/100 g mirr' in oxygen delivery for each increase of 1 ml/100 g min" 1 in cardiac oxygen consumption. Under these circumstances, myocardial oxygen extraction increased and coronary venous oxygen content fell. After a-receptor blockade, either intracoronary norepinephrine infusion or a carotid sinus reflex resulted in an increase of 1.23 ml/100 g min ' in oxygen delivery for each increase of 1 ml/100 g min' 1 in cardiac oxygen consumption. Myocardial oxygen extraction and coronary venous oxygen content changed only slightly after a-receptor blockade. The greater coronary vasodilation and lesser change in cardiac oxygen extraction after a-receptor blockade were significantly different (P < 0.001) from the values before blockade. It is concluded that the coronary a-receptor constrictor mechanism competes with metabolic vasodilation during sympathetic activation even when there are large increases in myocardial metabolism. The net effect of the a-receptor constrictor influence is to restrict the metabolically related flow increase by about 30%, thus increasing oxygen extraction and decreasing coronary venous oxygen content.