Document Detail


Increased inactivation of nitric oxide is involved in coronary endothelial dysfunction in heart failure.
MedLine Citation:
PMID:  11123219     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent evidence suggests the possibility that enhanced inactivation of endothelium-derived nitric oxide (NO) by oxygen free radical (OFR) may cause endothelial dysfunction in heart failure (HF). To test this hypothesis, we examined the effect of antioxidant therapy on endothelium-dependent vasodilation of the coronary circulation in a canine model of tachycardia-induced HF. Endothelium-dependent vasodilation was less than that in controls, and OFR formation in coronary arterial and myocardial tissues was greater in HF dogs than those in controls. The immunohistochemical staining of 4-hydroxy-2-nonenal, OFR-induced lipid peroxides was detected in coronary microvessels of HF dogs. Intracoronary infusion of the cell-permeable OFR scavenger Tiron inhibited OFR formation and improved endothelium-dependent vasodilation in HF dogs but not in controls. The NO synthesis inhibitor N(G)-monomethyl-L-arginine (L-NMMA) diminished the beneficial effect of Tiron in HF dogs. Endothelium-independent vasodilation was similar between control and HF dogs, and no change in its response was noted by Tiron or Tiron plus L-NMMA in either group. In summary, antioxidant treatment with Tiron improved coronary vascular endothelium-dependent vasodilation by increasing NO activity in tachycardia-induced HF. Thus coronary endothelial dysfunction in HF may be, at least in part, due to increased inactivation of NO by OFR.
Authors:
K Arimura; K Egashira; R Nakamura; T Ide; H Tsutsui; H Shimokawa; A Takeshita
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  280     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2001 Jan 
Date Detail:
Created Date:  2001-02-02     Completed Date:  2001-02-02     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H68-75     Citation Subset:  IM    
Affiliation:
Department of Cardiovascular Medicine, Kyushu University Graduate School of Medicine, Fukuoka, 812-8582 Japan.
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MeSH Terms
Descriptor/Qualifier:
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt / pharmacology
Acetylcholine / pharmacology
Animals
Coronary Vessels / physiopathology*
Dogs
Echocardiography
Electric Stimulation
Endothelium, Vascular / physiopathology*
Enzyme Inhibitors / pharmacology
Free Radicals / metabolism
Heart Failure / physiopathology*
Hemodynamics / drug effects
Immunohistochemistry
Indicators and Reagents
Lipid Peroxidation
Nitric Oxide / metabolism,  physiology*
Nitric Oxide Synthase / antagonists & inhibitors
Nitric Oxide Synthase Type III
omega-N-Methylarginine / pharmacology
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Free Radicals; 0/Indicators and Reagents; 10102-43-9/Nitric Oxide; 149-45-1/1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt; 17035-90-4/omega-N-Methylarginine; 51-84-3/Acetylcholine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type III

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


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