Presentation of venous endothelial function in the forearm venous capacitance bed of patients with chronic heart failure despite arterial endothelialdysfunction

Citation
Ak. Nightingale et al., Presentation of venous endothelial function in the forearm venous capacitance bed of patients with chronic heart failure despite arterial endothelialdysfunction, J AM COL C, 37(4), 2001, pp. 1062-1068
Citations number
41
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
0735-1097 → ACNP
Volume
37
Issue
4
Year of publication
2001
Pages
1062 - 1068
Database
ISI
SICI code
0735-1097(20010315)37:4<1062:POVEFI>2.0.ZU;2-S
Abstract
OBJECTIVES The goal of this study was to assess whether endothelial dysfunc tion occurs in the forearm venous capacitance bed of patients with chronic heart failure (CHF) and to determine the role of nitric oxide (NO) in modul ating venous tone. BACKGROUND Control of venous tone is crucially important in CHF. More than 70% of blood volume lies in thr venous capacitance beds. Therefore, small c hanges in venous tone may markedly affect cardiac filling pressures and car diac output. METHODS Venous tone was measured using radionuclide forearm venous plethysm ography 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-ar ginine 12 mg/min and stimulated NO using carbachol 15 mug/min. Brachial art ery flow-mediated dilation was assessed by ultrasonic wall-tracking. RESULTS Blockade of basal NO release caused a significant and similar venoc onstriction in patients (9.6 +/- 1.8%, p < 0.01) and controls (6.6 <plus/mi nus> 1.7%, p < 0.01). Carbachol-induced venodilation was significant and si milar in patients (36.8 <plus/minus> 3.9%, p < 0.001) and controls (40.7 <p lus/minus> 3.9%, p < 0.001). Brachial artery flow-mediated dilation was imp aired in patients compared with controls (2.0 <plus/minus> 0.6% vs. 7.5 +/- 2.5%, p < 0.01). CONCLUSIONS Our data indicate that, despite marked impairment uf the functi on of the arterial endothelium, there is preservation of both basal and sti mulated NO release in the forearm venous capacitance bed. This may provide important insights into mechanisms of endothelial dysfunction in CHF and th r potential for novel therapy. (J Am Coll Cardiol 2001;37:1062-8) (C) 2001 by the American College of Cardiology.