Document Detail


Preservation of venous endothelial function in the forearm venous capacitance bed of patients with chronic heart failure despite arterial endothelial dysfunction.
MedLine Citation:
PMID:  11263609     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: The goal of this study was to assess whether endothelial dysfunction occurs in the forearm venous capacitance bed of patients with chronic heart failure (CHF) and to determine the role of nitric oxide (NO) in modulating venous tone. BACKGROUND: Control of venous tone is crucially important in CHF. More than 70% of blood volume lies in the venous capacitance beds. Therefore, small changes in venous tone may markedly affect cardiac filling pressures and cardiac output. METHODS: Venous tone was measured using radionuclide forearm venous plethysmography in 24 patients with CHF and 16 age-matched controls. The effect of basal NO activity on venous tone was assessed by infusing N-monomethyl-L-arginine 12 mg/min and stimulated NO using carbachol 15 microg/min. Brachial artery flow-mediated dilation was assessed by ultrasonic wall-tracking. RESULTS: Blockade of basal NO release caused a significant and similar venoconstriction in patients (9.6 +/- 1.8%, p < 0.01) and controls (6.6 +/- 1.7%, p < 0.01). Carbachol-induced venodilation was significant and similar in patients (36.8 +/- 3.9%, p < 0.001) and controls (40.7 +/- 3.9%, p < 0.001). Brachial artery flow-mediated dilation was impaired in patients compared with controls (2.0 +/- 0.6% vs. 7.5 +/- 2.5%, p < 0.01). CONCLUSIONS: Our data indicate that, despite marked impairment of the function of the arterial endothelium, there is preservation of both basal and stimulated NO release in the forearm venous capacitance bed. This may provide important insights into mechanisms of endothelial dysfunction in CHF and the potential for novel therapy.
Authors:
A K Nightingale; D J Blackman; G R Ellis; M Schmitt; J A Morris-Thurgood; E A Jones; M P Frenneaux
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  37     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2001 Mar 
Date Detail:
Created Date:  2001-03-23     Completed Date:  2001-04-05     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:  1062-8     Citation Subset:  AIM; IM    
Affiliation:
Department of Cardiology, University of Wales College of Medicine, Cardiff, United Kingdom.
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MeSH Terms
Descriptor/Qualifier:
Aged
Arteries / physiopathology
Carbachol / pharmacology
Chronic Disease
Endothelium, Vascular / metabolism,  physiopathology*
Enzyme Inhibitors / pharmacology
Female
Forearm / blood supply
Heart Failure / physiopathology*
Humans
Male
Middle Aged
Nitric Oxide / metabolism
Nitric Oxide Synthase / antagonists & inhibitors
Vascular Capacitance*
Vasodilation
Veins / physiopathology*
omega-N-Methylarginine / pharmacology
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 51-83-2/Carbachol; EC 1.14.13.39/Nitric Oxide Synthase

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


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