Document Detail


Effects of intravenous dobutamine on coronary vasomotion in humans.
MedLine Citation:
PMID:  14607445     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: We sought to investigate the vascular mechanisms of dobutamine-induced myocardial ischemia. BACKGROUND: Dobutamine stress is often used as a surrogate for exercise. The effects of dobutamine on the epicardial arteries are incompletely understood and possibly different from those of physical exercise. METHODS: Intravenous (IV) dobutamine (40 microg/kg per min) was administered in 19 patients with normal, 23 patients with mildly atherosclerotic, and 12 patients with stenotic coronary arteries. In another two groups of patients with stenotic arteries, IV dobutamine was preceded by 1) an intracoronary (IC) bolus of the alpha-adrenergic blocker phentolamine (12 microg/kg, n = 12); and 2) an IC infusion of the nitric oxide substrate L-arginine (150 micromol/l per min for 20 min, n = 11). Intravenous saline instead of dobutamine was infused into eight patients with normal arteries. After dobutamine (or saline), an IC bolus of isosorbide dinitrate (ISDN, 0.2 mg) was given. Coronary vasomotion was evaluated by quantitative coronary angiography on angiograms obtained after each dose of dobutamine, saline, phentolamine, L-arginine, and ISDN. RESULTS: Dobutamine increased the rate-pressure product and heart rate similarly in all patients except those who received saline. Dobutamine induced vasodilation in normal (change in luminal diameter [DeltaLD] vs. baseline: 19 +/- 2%) and in mildly atherosclerotic arteries (DeltaLD: 8 +/- 2%, p < 0.05 vs. normal). In stenotic arteries, dobutamine did not induce significant vasomotion (DeltaLD: -3 +/- 3%); the latter was improved by L-arginine (DeltaLD: 10 +/- 3%, p < 0.05 vs. stenotic arteries) and fully restored by phentolamine (DeltaLD: 19 +/- 3%, p < 0.05 vs. stenotic arteries). CONCLUSIONS: Endothelial dysfunction and enhanced alpha-adrenergic tone contribute to the loss of dobutamine-induced vasodilation in coronary atherosclerosis. In contrast to physical exercise, dobutamine does not induce "paradoxical vasoconstriction" of atherosclerotic coronary arteries.
Authors:
Emanuele Barbato; Jozef Bartunek; Eric Wyffels; William Wijns; Guy R Heyndrickx; Bernard De Bruyne
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  42     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2003 Nov 
Date Detail:
Created Date:  2003-11-10     Completed Date:  2003-12-04     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1596-601     Citation Subset:  AIM; IM    
Affiliation:
Cardiovascular Center, OLV Ziekenhuis, Aalst, Belgium.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Agonists / pharmacology*
Arteriosclerosis / physiopathology
Coronary Stenosis / physiopathology
Coronary Vessels / drug effects,  physiology*
Dobutamine / pharmacology*
Dose-Response Relationship, Drug
Endothelium, Vascular / physiology
Female
Hemodynamics / drug effects
Humans
Male
Receptors, Adrenergic, alpha / physiology
Vasodilation / drug effects*
Chemical
Reg. No./Substance:
0/Adrenergic beta-Agonists; 0/Receptors, Adrenergic, alpha; 34368-04-2/Dobutamine
Comments/Corrections
Comment In:
J Am Coll Cardiol. 2003 Nov 5;42(9):1602-4   [PMID:  14607446 ]

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


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