| Vagal modulation of epicardial coronary artery size in dogs. A two-dimensional intravascular ultrasound study. | |
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MedLine Citation:
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PMID: 7554214 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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 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. |
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Authors:
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J A Kovach; J S Gottdiener; R L Verrier |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Circulation Volume: 92 ISSN: 0009-7322 ISO Abbreviation: Circulation Publication Date: 1995 Oct |
Date Detail:
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Created Date: 1995-11-14 Completed Date: 1995-11-14 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0147763 Medline TA: Circulation Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 2291-8 Citation Subset: AIM; IM |
Affiliation:
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Department of Medicine, Georgetown University Hospital and School of Medicine, Washington, DC, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Animals Cardiac Pacing, Artificial Coronary Vessels / innervation*, physiology, ultrasonography* Dogs Female Glycopyrrolate / pharmacology Heart Rate / physiology Male Muscarinic Antagonists / pharmacology Receptors, Muscarinic / drug effects, physiology Stellate Ganglion / physiology Ultrasonography, Interventional / methods* Vagotomy Vagus Nerve / physiology* Vasodilation / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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HL-33567/HL/NHLBI NIH HHS; HL-50078/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Muscarinic Antagonists; 0/Receptors, Muscarinic; 51-84-3/Acetylcholine; 596-51-0/Glycopyrrolate |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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