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

Abstract

The role of .alpha.-receptor constriction of coronary vessels in response to cardiac sympathetic activation was evaluated in closed-chest, chloralose-anesthetized dogs. Cardiac sympathetic activation was produced directly by intracoronary norepinephrine infusion at several different rates and reflexly by carotid sinus hypotension. The resulting changes in coronary blood flow and myocardial O2 consumption were recorded before and after .alpha.-receptor blockade with dibozane (3.0 mg/kg, i.v.) or phenoxybenzamine (0.5 mg/kg, intracoronary). The changes in coronary blood flow were normalized to changes in myocardial metabolism by division of the O2 delivery (coronary flow times arterial O2 content) by the change in myocardial O2 consumption per 100 g of myocardium. Before .alpha.-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 min-1 in O2 delivery for each increase of 1 ml/100 g min-1 in cardiac O2 consumption. Under these circumstances myocardial O2 extraction increased, and coronary venous O2 content fell. After .alpha.-receptor blockade either intracoronary norepinephrine infusion or a carotid sinus reflex resulted in an increase of 1.23 ml/100 g min-1 in O2 delivery for each increase of 1 ml/100 g min-1 in cardiac O2 consumption. Myocardial O2 extraction and coronary venous O2 content changed only slightly after .alpha.-receptor blockade. The greater coronary vasodilation and lesser change in cardiac O2 extraction after .alpha.-receptor blockade were significantly different (P < 0.001) from the values before blockade. The coronary .alpha.-receptor constrictor mechanism competes with metabolic vasodilation during sympathetic activation even when there are large increases in myocardial metabolism. The net effect of the .alpha.-receptor constrictor influence is to restrict the metabolically related flow increase by about 30%, thus increasing O2 extraction and decreasing coronary venous O2 content.