Document Detail


Catecholamine effects on cardiac remodelling, oxidative stress and fibrosis in experimental heart failure.
MedLine Citation:
PMID:  12189044     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The aim of the study was to assess the relationships between oxidative stress, cardiac remodelling and fibrosis on an experimental model of heart failure with adrenergic stimulation. Large myocardial infarction (approximately 50% of the left ventricle myocardium) was obtained by ligation of the left coronary artery of normotensive male Wistar rats. Sham animals were submitted to left thoracotomy without coronary ligation. In order to perform cardiac stimulation by catecholamines, mini-osmotic pumps were implanted in animals 10 weeks after surgery to deliver noradrenalin for a 2-week period. At the end of this period, the following investigations were performed: haemodynamics, morphometry, fibrosis quantification, plasma and tissue catecholamine assay and oxidative stress status. Coronary ligation induced dilatation of left ventricle with compensatory hypertrophy of the right ventricle and of the remaining left ventricle myocardium. This remodelling process was associated in non-infarcted myocardium with increased collagen infiltration and increased oxidative stress. Ten weeks after surgery, the chronic administration of noradrenalin for 2 weeks did not increase oxidative stress. Noradrenalin, however, induced inotropic stimulation and myocardial hypertrophy, but to a lesser extent in infarcted rats compared to sham rats. Our results suggest that noradrenalin infusion to levels in excess of those seen post-infarction is associated with fibrosis and oxidative stress. Moreover, noradrenalin in infarcted animals caused additional fibrosis without further increasing oxidative stress. The mechanism of catecholamine-induced fibrosis may thus involve different processes such as ischaemia, increased mechanical stress, cytokines and neurohormones.
Authors:
Dominique Bonnefont-Rousselot; Allal Mahmoudi; Nathalie Mougenot; Odile Varoquaux; Gilles Le Nahour; Pierre Fouret; Philippe Lechat
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Redox report : communications in free radical research     Volume:  7     ISSN:  1351-0002     ISO Abbreviation:  Redox Rep.     Publication Date:  2002  
Date Detail:
Created Date:  2002-08-21     Completed Date:  2003-02-12     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9511366     Medline TA:  Redox Rep     Country:  England    
Other Details:
Languages:  eng     Pagination:  145-51     Citation Subset:  IM    
Affiliation:
Laboratoire de Biochimie B, Coeur et Vaisseaux, Groupe Hospitalier Pitié-Salpêtrière (AP-HP), 47 boulevard de l'Hôpital, 75651 Paris Cedex 13, France. dominique.rousselot@psl.ap-hop-paris.fr
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MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal
Echocardiography
Fibrosis
Heart / drug effects,  physiopathology*
Heart Failure / physiopathology*
Hemodynamics / physiology*
Male
Myocardial Infarction / physiopathology*
Myocardium / metabolism,  pathology
Norepinephrine / pharmacology*
Oxidative Stress / drug effects*
Rats
Rats, Wistar
Thiobarbituric Acid Reactive Substances / metabolism
Chemical
Reg. No./Substance:
0/Thiobarbituric Acid Reactive Substances; 51-41-2/Norepinephrine

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