Vagal modulation of epicardial coronary artery size in dogs. A two-dimensional intravascular ultrasound study.
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.


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 micrograms/kg i.v.), 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.
Kovach
J A
JA
Department of Medicine, Georgetown University Hospital and School of Medicine, Washington, DC, USA.
Gottdiener
J S
JS
Verrier
R L
RL
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002304:Cardiac Pacing, Artificial; D003331:Coronary Vessels / Q000000981:diagnostic imaging* / Q000294:innervation* / Q000502:physiology; D004285:Dogs; D005260:Female; D006024:Glycopyrrolate / Q000494:pharmacology; D006339:Heart Rate / Q000502:physiology; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D011976:Receptors, Muscarinic / Q000187:drug effects / Q000502:physiology; D013233:Stellate Ganglion / Q000502:physiology; D018084:Ultrasonography, Interventional / Q000379:methods*; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*
D018727:Muscarinic Antagonists; D011976:Receptors, Muscarinic; D000109:Acetylcholine; D006024:Glycopyrrolate