Alpha-receptor constriction induced by atrial fibrillation during maximal coronary dilatation.

The mechanism of coronary vasoconstriction induced by atrial fibrillation during maximal coronary dilatation was studied in 19 chloralose-urethane anesthetized dogs. Maximal coronary dilatation was achieved by carbochromene (5 mg/kg i.v.) or dipyridamole (0.2 mg/kg i.v.). Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Atrial fibrillation was compared with rhythmic atrial pacing at similar heart rates (207 +/- 12 vs. 204 +/- 12 beats/min). During maximal coronary dilatation, coronary resistance was 0.38 +/- 0.05 mm Hg X min X 100 g/ml (RU) at sinus rhythm, 0.41 +/- 0.06 RU at atrial pacing, and 0.52 +/- 0.07 RU at atrial fibrillation, that was significantly (p less than 0.005) higher than during sinus rhythm and atrial pacing. Accordingly, coronary oxygen extraction was 14 +/- 1% at sinus rhythm, 17 +/- 1% at atrial pacing (p less than 0.005 vs. sinus rhythm) and 27 +/- 2% at atrial fibrillation (p less than 0.001 vs sinus rhythm and atrial pacing). Beta-adrenoceptor blockade with propranolol (1 mg/kg i.v.) did not prevent this coronary vasoconstrictive effect. Following alpha-blockade with phenoxybenzamine (10 mg/kg i.v.), however, coronary resistance was 0.52 +/- 0.08 RU during sinus rhythm, 0.54 +/- 0.10 RU during atrial pacing and 0.57 +/- 0.09 RU during atrial fibrillation. The data suggest coronary vasoconstriction induced by atrial fibrillation mediated by an alpha-adrenoceptor mechanism.