Alpha-receptor restriction of coronary blood flow during atrial fibrillation

Abstract

The effects of atrial fibrillation (AF) on coronary circulation before and after alpha-receptor blockade were studied in 14 anesthetized, open-chest dogs. AF was induced by electrical stimulation of the left atrial appendage; identical rhythmic heart rates were adjusted by left atrial pacing. During atrial pacing, coronary vascular resistance (CVR) was 0.97 ± 0.10 mm Hg × min × 100 g/ml (resistance units [RU]), coronary blood flow (CBF) 125 ± 14 ml/min × 100 g, and oxygen saturation 30 ± 2%; plasma epinephrine was 193 ± 42 pg/ml and norepinephrine 584 ± 111 pg/ml. During AF, CVR was higher (1.16 ± 0.11 RU, p < 0.0005), whereas CBF (92 ± 9 ml/min × 100 g, p < 0.001) and coronary sinus oxygen saturation (24 ± 2%, p < 0.0025) were lower than during atrial pacing. When AF was induced, epinephrine increased to 333 ± 98 pg/ml (p < 0.05) and norepinephrine to 1,005 ± 214 pg/ml (p < 0.005). The large increase in plasma catecholamines suggested an activation of the sympathoadrenal system during AF. In addition, the alphareceptor blocker phenoxybenzamine (10 mg/kg, intravenously) abolished the differences in CVR, CBF and oxygen saturation between AF and atrial pacing. The data suggest that the decrease in CBF and increase in CVR during experimentally induced AF are caused by coronary vasoconstriction, mediated by sympathetic activation of alpha receptors in the coronary vascular bed.