Titre
Endothelial dysfunction in chronic heart failure. Experimental and clinical studies
Type
synthèse (review)
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Arzneimittel-Forschung
Auteur(s)
Drexler, H.
Auteure/Auteur
Hayoz, D.
Auteure/Auteur
Munzel, T.
Auteure/Auteur
Just, H.
Auteure/Auteur
Zelis, R.
Auteure/Auteur
Brunner, H. R.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
0004-4172
Statut éditorial
Publié
Date de publication
1994-03
Volume
44
Numéro
3A
Première page
455
Dernière page/numéro d’article
8
Notes
In Vitro
Journal Article
Review --- Old month value: Mar
Journal Article
Review --- Old month value: Mar
Résumé
The endothelium plays an important role in the control of human vascular tone by releasing endothelium-derived nitric oxide. Therefore, endothelial dysfunction could be involved in the increased peripheral vasoconstriction of patients with chronic congestive heart failure (CHF). To investigate endothelial function in humans in vivo, agents such as acetylcholine are used to stimulate the release of endothelium-derived nitric oxide (EDRF). Conversely, N-mono-methyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide synthesis from L-arginine decreases forearm blood flow by inhibiting the basal release of nitric oxide. Consistent with experimental studies, the blood flow response to acetylcholine is blunted in patients with chronic heart failure as compared to healthy age-matched volunteers. In contrast, the decrease in blood flow induced by L-NMMA appears to be exaggerated in CHF. The blood flow response to nitroglycerin or sodium nitroprusside, endothelium-independent vasodilators, is usually preserved in patients with chronic, non-edematous heart failure, indicating a normal response of the vascular smooth muscle of resistance vessels to exogenous nitric oxide. In contrast, the dilator response of the radial artery diameter to nitroglycerin and flow-dependent dilation are impaired in patients with chronic heart failure, indicating that the abnormal flow-mediated relaxation of large arteries may be due to both endothelial and vascular smooth muscle alterations. Thus, impaired endothelium-dependent dilation of peripheral resistance vessels emerges in chronic heart failure, suggesting a reduced release of nitric oxide upon stimulation. Thus, endothelial dysfunction may be involved in the impaired vasodilator capacity in the peripheral circulation, e.g. during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
Sujets
PID Serval
serval:BIB_C5859E7704D3
PMID
Date de création
2008-01-17T15:38:09.697Z
Date de création dans IRIS
2025-05-21T01:55:04Z