Linked Life Data

12450571

Source:http://linkedlifedata.com/resource/pubmed/id/12450571

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-11-26
pubmed:abstractText
The aim of our study was to analyse the mechanisms underlying cardiac toxicity caused by beta-adrenoceptor stimulation and the relationships with their associated downregulation during heart failure. We used the experimental model of coronary artery ligation-induced myocardial infarction in male Wistar rats. In order to increase beta-adrenergic stimulation, rats were subjected to a 15-day chronic isoprenaline administration (30 microg/kg/h). Isoprenaline administration induced haemodynamic inotropic compensation, almost abolished in vitro inotropic response to isoprenaline on papillary muscle (P<0.005) but promoted fibrosis. Isoprenaline treatment markedly reduced the B(max) of beta(2)-adrenoceptors (by 53% in sham and 44% in infarcted rats) but not that of beta(1)-adrenoceptors. These results suggest that beta(1)-adrenoceptors rather than beta(2)-adrenoceptors underlie the deleterious effects of chronic beta-adrenergic stimulation on cardiac fibrosis and are in agreement with the demonstrated benefit induced in human heart failure by beta(1)-adrenoceptor antagonists.
pubmed:language
eng
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:author
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
69-75
pubmed:dateRevised
2006-11-15
pubmed:articleTitle
Toxic cardiac effects of catecholamines: role of beta-adrenoceptor downregulation.
pubmed:affiliation
Service de Pharmacologie, Hôpital de la Pitié-Salpêtrière, Paris, France.