Endothelial function in congestive heart failure

Details

Serval ID
serval:BIB_B4318830E303
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Endothelial function in congestive heart failure
Journal
American Heart Journal
Author(s)
Drexler  H., Hayoz  D., Munzel  T., Just  H., Zelis  R., Brunner  H. R.
ISSN
0002-8703 (Print)
Publication state
Published
Issued date
09/1993
Volume
126
Number
3 Pt 2
Pages
761-4
Notes
Journal Article
Review --- Old month value: Sep
Abstract
There is evidence that the endothelium plays an important role in the control of human vascular tone by releasing endothelium-derived nitric oxide and, therefore, a defective endothelial function could be involved in the increased peripheral vasoconstriction of patients with chronic congestive heart failure. To investigate endothelial function in humans in vivo, agents such as acetylcholine, a short-acting stimulator of the release of endothelium-derived nitric oxide, has been used. Conversely, N-mono-methyl-L-arginine, a specific inhibitor of nitric oxide synthesis from L-arginine, has recently been shown to decrease blood flow during infusion into the brachial artery of healthy volunteers (control subjects) 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 compared with healthy age-matched volunteers. In contrast, the decrease in blood flow induced by N-mono-methyl-L-arginine appears to be exaggerated in congestive heart failure. The blood flow response to nitroglycerin or sodium nitroprusside, endothelium-independent vasodilators, is usually preserved in patients with chronic, nonedematous 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 is impaired in patients with chronic heart failure, indicating that the abnormal flow-mediated relaxation of large arteries may be caused by both endothelial and structural abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
Keywords
Animals Chronic Disease Endothelium, Vascular/metabolism/*physiopathology Heart Failure, Congestive/*physiopathology Humans Nitric Oxide/*metabolism Vasoconstriction/physiology
Pubmed
Web of science
Create date
17/01/2008 16:38
Last modification date
20/08/2019 15:22
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