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Titolo:
In vivo myocardial protection from ischemia/reperfusion injury by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone
Autore:
Yue, TL; Chen, J; Bao, WK; Narayanan, PK; Bril, A; Jiang, W; Lysko, PG; Gu, JL; Boyce, R; Zimmerman, DM; Hart, TK; Buckingham, RE; Ohlstein, EH;
Indirizzi:
GlaxoSmithKline Pharmaceut, Dept Cardiovasc Pharmacol, King Of Prussia, PA19406 USA GlaxoSmithKline Pharmaceut King Of Prussia PA USA 19406 ssia, PA19406 USA GlaxoSmithKline Pharmaceut, Dept Safety Assessment, King Of Prussia, PA 19406 USA GlaxoSmithKline Pharmaceut King Of Prussia PA USA 19406 sia, PA 19406 USA
Titolo Testata:
CIRCULATION
fascicolo: 21, volume: 104, anno: 2001,
pagine: 2588 - 2594
SICI:
0009-7322(20011120)104:21<2588:IVMPFI>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
MONOCYTE CHEMOATTRACTANT PROTEIN-1; ISCHEMIA-REPERFUSION INJURY; DIABETIC-PATIENTS; PPAR-GAMMA; INFARCTION; NEUTROPHIL; RATS; TROGLITAZONE; MECHANISMS; EXPRESSION;
Keywords:
ischemia; myocardial infarction; diabetes; PPAR-gamma; rosiglitazone;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Yue, TL GlaxoSmithKline Pharmaceut, Dept Cardiovasc Pharmacol, 709 Swedeland Rd,POB 1539,UW2510, King Of Prussia, PA 19406 USA GlaxoSmithKline Pharmaceut 709 Swedeland Rd,POB 1539,UW2510 King Of Prussia PA USA 19406
Citazione:
T.L. Yue et al., "In vivo myocardial protection from ischemia/reperfusion injury by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone", CIRCULATION, 104(21), 2001, pp. 2588-2594

Abstract

Background-Diabetes is associated with increased risk of mortality as a consequence of acute myocardial infarction. This study determined whether rosiglitazone (ROSI) could reduce myocardial infarction after ischemia/reperfusion injury. Methods and Results-Male Lewis rats were anesthetized, and the left anterior descending coronary artery was ligated for 30 minutes. After reperfusionfor 24 hours, the ischemic and infarct sizes were determined. ROSI at 1 and 3 mg/kg IV reduced infarct size by 30% and 37%, respectively (P <0.01 versus vehicle). Pretreatment with ROSI (3 mg (.) kg(-1) (.) d(-1) PO) for 7 days also reduced infarct size by 24% (P <0.01). ROSI also improved ischemia/reperfusion-induced myocardial contractile dysfunction. Left ventricular systolic pressure and positive and negative maximal values of the first derivative of left ventricular pressure (dP/dt) were significantly improved in ROSI-treated rats. ROSI reduced the accumulation of neutrophils and macrophages in the ischemic heart by 40% and 43%, respectively (P <0.01). Ischemia/reperfusion induced upregulation of CD11b/CD18 and downregulation of L-selectin on neutrophils and monocytes; these effects were significantly attenuated in ROSI-treated animals. Likewise, intercellular adhesion molecule-1 expression in ischemic hearts was markedly diminished by ROSI, as was the ischemia/reperfusion-stimulated upregulation of monocyte chemoattractant protein-1. Conclusions-ROSI reduced myocardial infarction and improved contractile dysfunction caused by ischemia/reperfusion injury. The cardioprotective effect of ROSI was most likely due to inhibition of the inflammatory response.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 12:28:50