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Titolo:
Pretreating rats with hyperoxia attenuates ischemia-reperfusion injury of the heart
Autore:
Tahepold, P; Valen, G; Starkopf, J; Kairane, C; Zilmer, M; Vaage, J;
Indirizzi:
Karolinska Hosp, Crafoord Lab Expt Surg, S-17176 Stockholm, Sweden Karolinska Hosp Stockholm Sweden S-17176 Surg, S-17176 Stockholm, Sweden Karolinska Hosp, Dept Thorac Surg, S-17176 Stockholm, Sweden Karolinska Hosp Stockholm Sweden S-17176 Surg, S-17176 Stockholm, Sweden Univ Tartu, Inst Biochem, EE-50090 Tartu, Estonia Univ Tartu Tartu Estonia EE-50090 Inst Biochem, EE-50090 Tartu, Estonia
Titolo Testata:
LIFE SCIENCES
fascicolo: 14, volume: 68, anno: 2001,
pagine: 1629 - 1640
SICI:
0024-3205(20010223)68:14<1629:PRWHAI>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
OXIDATIVE STRESS; NORMOBARIC HYPEROXIA; HYDROGEN-PEROXIDE; LATE-PHASE; PROTEIN; PROTECTION; RESISTANCE; ADENOSINE; SYNTHASE;
Keywords:
ischemia-reperfusion injury; cardioprotection; hyperoxia; oxidative stress;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
22
Recensione:
Indirizzi per estratti:
Indirizzo: Valen, G Karolinska Hosp, Crafoord Lab Expt Surg, L6 00, S-17176 Stockholm, Sweden Karolinska Hosp L6 00 Stockholm Sweden S-17176 Stockholm, Sweden
Citazione:
P. Tahepold et al., "Pretreating rats with hyperoxia attenuates ischemia-reperfusion injury of the heart", LIFE SCI, 68(14), 2001, pp. 1629-1640

Abstract

Oxidative stress may precondition the heart. The present study investigated whether hyperoxia elicits a preconditioning-like response. Rats were kept in a hyperoxic (>95% O-2) environment for 60 or 180 minutes. Hearts were Langendorff-perfused immediately or 24 hours after hyperoxia,and exposed to 25 minutes of global ischemia and 60 minutes of reperfusion. Whole blood was sampled after 60 and 180 minutes of hyperoxia for oxidative stress markers. Hearts were sampled immediately or 24 hours after hyperoxia for measurement of antioxidants, lipid peroxidation products, heat shock protein 72 and endothelial nitric oxide synthase. At the end of reperfusion after 1 h hyperoxia, infarct size was determined by tetrazolium staining. Hyperoxia increased serum levels of conjugated dienes, reduced serum antioxidative protection, reduced reperfusion arrhythmias in most groups, and improved myocardial function. Infarct size was reduced from 45% of myocardial tissue in controls to 22% in treated animals. The myocardial activity of antioxidant enzymes, content of heat shock protein 72, and endothelial nitric oxide synthase in myocardial tissue were not influenced. In conclusion, hyperoxia induces a low-graded systemic oxidative stress, improves postischemic cardiac function and reduces infarct size. The mediators of protection remain to be determined. (C) 2001 Elsevier Science Inc.Allrights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 09:39:49