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Titolo:
The role of the endothelium for reperfusion injury
Autore:
Pernow, J; Gonon, AT; Gourine, A;
Indirizzi:
Karolinska Hosp, Dept Cardiol, S-17176 Stockholm, Sweden Karolinska Hosp Stockholm Sweden S-17176 diol, S-17176 Stockholm, Sweden
Titolo Testata:
EUROPEAN HEART JOURNAL SUPPLEMENTS
fascicolo: C, volume: 3, anno: 2001,
pagine: C22 - C27
SICI:
1520-765X(200106)3:C<C22:TROTEF>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
A-RECEPTOR ANTAGONIST; MYOCARDIAL ISCHEMIA-REPERFUSION; REDUCES INFARCT SIZE; NITRIC-OXIDE; L-ARGININE; MONOCLONAL-ANTIBODY; NEUTROPHIL DEPLETION; ADHESION MOLECULE-1; CORONARY-OCCLUSION; PROTECTS;
Keywords:
endothelium; reperfusion; nitric oxide; endothelin; neutrophils;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Pernow, J Karolinska Hosp, Dept Cardiol, S-17176 Stockholm, Sweden Karolinska Hosp Stockholm Sweden S-17176 176 Stockholm, Sweden
Citazione:
J. Pernow et al., "The role of the endothelium for reperfusion injury", EUR H J SUP, 3(C), 2001, pp. C22-C27

Abstract

Reperfusion following myocardial ischaemia induces a rapid change in endothelial function. Endothelium-dependent vasodilatation is impaired due to attenuated production of nitric oxide (NO) and/or enhanced inactivation of NOby superoxide. In addition, production of the vasoconstrictor peptide endothelin is increased. This results in a change from a state of vasorelaxation in the normal situation to an increased vasoconstrictor tone following reperfusion. There is a marked infiltration of neutrophils into the jeopardized myocardium during early reperfusion, which contributes to cell death. The adhesion of neutrophils to the endothelium is mediated by cell adhesion molecules which are expressed on endothelial cells, vascular smooth muscle cells and neutrophils during reperfusion. The reduction in NO bioavailability during early reperfusion contributes to several events in the reperfusioninjury. Therefore, maintenance of NO levels is important for protection against reperfusion injury. Administration of the NO substrate L-arginine or NO donors in connection with reperfusion attenuates neutrophil accumulationand reduces infarct size. Furthermore, blockade of adhesions molecules reduces the extent of reperfusion injury. Endothelin also seems to be of importance for the development of reperfusion injury. Endothelin receptor antagonists improve endothelial and ventricular; function and reduce infarct sizefollowing ischaemia and reperfusion. The mechanism behind the cardioprotective effect of endothelin receptor antagonists seems to involve inhibition of neutrophil-mediated injury and NO production. The endothelium plays an important role during the development of reperfusion injury. The reperfusioninjury is reduced by enhancing NO levels, blocking endothelin receptors and inhibiting neutrophil adhesion. (C) 2001 The European Society of Cardiology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 11:38:11