Adrenergic Coronary Vasoconstriction in the Presence of Coronary Stenosis in the Dog

Previous studies have demonstrated competition between sympathetic α receptor-mediated coronary vasoconstriction and local metabolic vasodilation during sympathetic activation. The present study tested if this competition also occurs in the presence of coronary stenosis. In closed-chest dogs, the le...

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Bibliographic Details
Published in:Circulation research 1981-03, Vol.48 (3), p.416-423
Main Authors: BUFFINGTON, CHARLES W, FEIGL, ERIC O
Format: Article
Language:English
Subjects:
Animals
Blood Pressure - drug effects
Coronary Circulation
Coronary Disease - physiopathology
Coronary Vessels - innervation
Coronary Vessels - physiopathology
Dogs
Heart Rate - drug effects
Lactates - blood
Norepinephrine - pharmacology
Oxygen - blood
Oxygen Consumption - drug effects
Sympathetic Nervous System - physiopathology
Vascular Resistance - drug effects
Vasoconstriction - drug effects
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Summary:Previous studies have demonstrated competition between sympathetic α receptor-mediated coronary vasoconstriction and local metabolic vasodilation during sympathetic activation. The present study tested if this competition also occurs in the presence of coronary stenosis. In closed-chest dogs, the left coronary artery was cannulated, and blood flow from the aorta was restricted by a moderate stenosis (70% area reduction). Intracoronary norepinephrine infusion produced coronary vascular α receptor and myocardial β receptor activation. Norepinephrine infusion was repeated following α receptor blockade with phenoxybenzamine (0.25 mg/kg, injected into the coronary artery). Myocardial oxygen and lactate extraction, coronary sinus blood oxygen tension, and coronary resistance were compared at equal levels of myocardial oxygen consumption before and after coronary α receptor blockade. In the presence of coronary stenosis, intracoronary norepinephrine infusion decreased coronary sinus oxygen content and increased myocardial oxygen extraction. At comparable myocardial oxygen consumptions coronary vascular resistance was greater with α receptors intact than after α receptor blockade. The increase in myocardial oxygen extraction was prevented by α receptor blockade. We conclude that a sympathetic α receptor-mediated coronary vasoconstrictor influence operates, even in the presence of coronary stenosis, to limit oxygen delivery to the heart and increase myocardial oxygen extraction up to the point of cardiac failure, but that this vasoconstrictor effect does not result in net myocardial lactate production. Circ Res 48416-423, 1981
ISSN:0009-7330
1524-4571
DOI:10.1161/01.res.48.3.416