Document Detail

Structural and functional assessment of small arteries in patients with chronic heart failure.
MedLine Citation:
PMID:  10585894     Owner:  NLM     Status:  MEDLINE    
The physiological response to a chronically failing heart is the implementation of compensatory mechanisms intended to support blood pressure. These mechanisms, which are not fully understood, increase peripheral vascular tone, thus increasing the strain on the weakened myocardium. This study investigated the structure and function of small arteries from heart failure patients and controls without heart failure in an attempt to identify abnormalities associated with heart failure which may be related to these mechanisms. Small arteries were dissected from gluteal biopsies and studied using wire myography. Arterial morphological parameters were measured and concentration-response curves constructed for a number of vasoconstrictor and vasodilator agonists. Plasma concentrations of neuroendocrine hormones were also measured. There were no morphological differences between small arteries from control subjects and those from patients with chronic heart failure. In heart failure patients, vasoconstrictor responses to endothelin-1 were significantly reduced, although plasma endothelin-1 levels were increased. Arteries from heart failure patients also showed evidence of an impaired neuronal uptake mechanism, since blockade by cocaine had no effect on noradrenaline-induced vasoconstriction in these vessels. These results suggest that small-artery structure is not altered in chronic heart failure and so cannot account for the heightened vascular resistance in this syndrome. However, abnormal neuronal uptake and impaired vasoconstriction in response to endothelin-1 may be associated with the complex compensatory phenomenon involved in heart failure.
C Hillier; P J Cowburn; J J Morton; H J Dargie; J G Cleland; J J McMurray; J C McGrath
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  97     ISSN:  0143-5221     ISO Abbreviation:  Clin. Sci.     Publication Date:  1999 Dec 
Date Detail:
Created Date:  2000-02-03     Completed Date:  2000-02-03     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  671-9     Citation Subset:  IM    
Department of Biological Sciences, Faculty of Health, Glasgow Caledonian University, Glasgow G4 0BA, Scotland, U.K.
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MeSH Terms
Acetylcholine / pharmacology
Analysis of Variance
Angiotensin II / blood,  pharmacology
Arteries / drug effects,  physiopathology
Bradykinin / pharmacology
Case-Control Studies
Dose-Response Relationship, Drug
Endothelin-1 / blood,  pharmacology
Epoprostenol / analogs & derivatives,  pharmacology
Heart Failure / blood,  pathology*,  physiopathology*
Middle Aged
Muscle, Skeletal / blood supply*
Natriuretic Peptide, Brain / blood
Nitroprusside / pharmacology
Norepinephrine / blood,  pharmacology
Vascular Resistance / drug effects*
Vasoconstrictor Agents / pharmacology
Vasodilator Agents / pharmacology
Reg. No./Substance:
0/Endothelin-1; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 11128-99-7/Angiotensin II; 114471-18-0/Natriuretic Peptide, Brain; 15078-28-1/Nitroprusside; 35121-78-9/Epoprostenol; 51-41-2/Norepinephrine; 51-84-3/Acetylcholine; 58-82-2/Bradykinin; 95722-07-9/cicaprost

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

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