Document Detail


Cholinergic modulation of the coronary vasoconstriction induced by cocaine in conscious dogs.
MedLine Citation:
PMID:  8443913     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The effects of cocaine on the coronary circulation were examined in conscious dogs chronically instrumented to measure arterial and left ventricular pressures, coronary blood flow, and arterial and coronary sinus oxygen content. METHODS AND RESULTS: With heart rate held constant, the peak effects of cocaine (1 mg/kg i.v.) occurred within 2 minutes, when mean arterial pressure increased by 42 +/- 5 mm Hg, coronary blood flow increased by 13 +/- 3%, and coronary vascular resistance increased by 24 +/- 3%. The arterial oxygen content increased significantly (by 2.8 +/- 0.3 vol%), the arterial-coronary sinus oxygen difference increased by 2.5 +/- 0.6 vol%, and myocardial oxygen consumption increased by 41 +/- 9%. The increase in coronary vascular resistance induced by cocaine was attenuated (p < 0.05) in the presence of cholinergic blockade (12 +/- 3%) despite a similar increase in MVO2 (49 +/- 8%). The increase in coronary vascular resistance was enhanced (p < 0.05) in the presence of beta-adrenergic receptor blockade (46 +/- 8%), whereas the MVO2 response was less (28 +/- 3%). Again, the addition of cholinergic blockade to beta-blockade attenuated the increase in coronary vascular resistance (23 +/- 6%) without affecting the increase in MVO2 (25 +/- 4%). Combined alpha-, beta-, and cholinergic blockades abolished the systemic hemodynamic and coronary vasoconstrictor response to cocaine. CONCLUSIONS: In conscious dogs, cocaine induces coronary vasoconstriction, which competes with coronary vasodilator responses to increases in myocardial oxygen consumption. The mechanisms of cocaine's coronary vascular effects are mediated via adrenergic stimulation, and the intensity of the vasoconstrictor effects was reduced significantly by cholinergic blockade, in both the presence and absence of beta-adrenergic receptor blockade.
Authors:
R P Shannon; B S Stambler; K Komamura; T Ihara; S F Vatner
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  87     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1993 Mar 
Date Detail:
Created Date:  1993-04-06     Completed Date:  1993-04-06     Revised Date:  2010-03-24    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  939-49     Citation Subset:  AIM; IM; S    
Affiliation:
Department of Medicine, Harvard Medical School, Boston, Mass.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cocaine / pharmacology*
Coronary Circulation / drug effects*,  physiology*
Dogs
Dose-Response Relationship, Drug
Female
Hemodynamics / drug effects
Male
Norepinephrine / pharmacology
Parasympathetic Nervous System / physiology*
Vasoconstriction / drug effects*,  physiology*
Grant Support
ID/Acronym/Agency:
HL-33107/HL/NHLBI NIH HHS; HL-38070/HL/NHLBI NIH HHS; RR-00168/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
50-36-2/Cocaine; 51-41-2/Norepinephrine
Comments/Corrections
Comment In:
Circulation. 1993 Mar;87(3):1046-7   [PMID:  8443884 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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