(Circulation. 1995;92:2291-2298.)
© 1995 American Heart Association, Inc.
Articles |
Vagal Modulation of Epicardial Coronary Artery Size in Dogs
A Two-Dimensional Intravascular Ultrasound Study
Presented in part at the 42nd Annual Scientific Session of the American College of Cardiology, Anaheim, Calif, March 14-18, 1993.
From the Department of Medicine, Division of Cardiology, and the Department of Pharmacology (R.L.V.), Georgetown University Hospital and School of Medicine, Washington, DC, and the Department of Medicine, Cardiovascular Division, New England Deaconess Hospital (R.L.V.), Harvard Medical School, Boston, Mass.
Correspondence to Richard L. Verrier, PhD, Institute for Prevention of Cardiovascular Disease, Deaconess Hospital, Harvard Medical School, 1 Autumn St, Boston, MA 02215.
Background Because the role of tonic vagus nerve activity in regulating conduit coronary artery size remains undefined, we investigated the response of epicardial coronary artery size to changes in resting vagal tone resulting from vagotomy and muscarinic receptor blockade.
Methods and Results Using intravascular ultrasound to measure left circumflex coronary artery cross-sectional area continuously, we examined the effects of vagotomy on left circumflex cross-sectional area in nine dogs. Lumen area decreased 20% from 8.70±2.81 to 6.92±1.97 mm2 after right vagotomy, 17% to 7.19±2.80 mm2 after left vagotomy (both P<.05 versus baseline), and 38% to 5.42±2.00 mm2 after bilateral vagotomy (P<.05 versus unilateral vagotomy). Vasoconstriction occurred despite increases in heart rate and an unchanged rate-pressure product. In six additional dogs, after acetylcholine (100 µg/kg IV), lumen area increased by 18%, although heart rate, blood pressure, and rate-pressure product were unchanged. Vasodilation was prevented by prior muscarinic blockade with glycopyrrolate. With glycopyrrolate administration and heart rate control by pacing, lumen area decreased by 26% (P=.011). When stellate stimulation was performed in a third group of eight dogs with heart rate, blood pressure, and rate-pressure product controlled by a combination of pacing and exsanguination, there was no change in coronary area, thus precluding reflex sympathetic activation as a contributor to the vasoconstriction produced by vagal withdrawal.
Conclusions Vagus nerve activity maintains tonic dilation of the left circumflex coronary artery by muscarinic receptor activation. Each vagus nerve contributes approximately equally to the tonically dilated state. Vagotomy-induced vasoconstriction occurs independently of local metabolic factors and coronary distending pressure and is a result of cholinergic withdrawal rather than reflex sympathetic activation.
Key Words: ultrasonics • vagus nerve • vasodilation • muscarinic receptors
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