Summary
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 Hgxminx100 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<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<0.005 vs. sinus rhythm) and 27±2% at atrial fibrillation (p<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.
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Supported by a grant from the Deutsche Forschungsgemeinschaft, Bonn, F.R.G.
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Ertl, G., Wichmann, J., Kaufmann, M. et al. Alpha-receptor constriction induced by atrial fibrillation during maximal coronary dilatation. Basic Res Cardiol 81, 29–39 (1986). https://doi.org/10.1007/BF01907425
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DOI: https://doi.org/10.1007/BF01907425