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Titolo:
Adenosine A(1) receptor activation induces delayed preconditioning in ratsmediated by manganese superoxide dismutase
Autore:
Dana, A; Jonassen, AK; Yamashita, N; Yellon, DM;
Indirizzi:
Univ Coll London Hosp, Hatter Inst & Ctr Cardiol, London WC1E 6DB, EnglandUniv Coll London Hosp London England WC1E 6DB , London WC1E 6DB, England Univ Coll London, Sch Med, London W1N 8AA, England Univ Coll London London England W1N 8AA Sch Med, London W1N 8AA, England
Titolo Testata:
CIRCULATION
fascicolo: 24, volume: 101, anno: 2000,
pagine: 2841 - 2848
SICI:
0009-7322(20000620)101:24<2841:AARAID>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; ISCHEMIA-REPERFUSION INJURY; PROTEIN-KINASE-C; SENSITIVE K+ CHANNELS; MYOCARDIAL PROTECTION; RABBIT HEART; 2ND WINDOW; ISCHEMIA/REPERFUSION INJURY; BIPHASIC CARDIOPROTECTION; SUBLETHAL ISCHEMIA;
Keywords:
adenosine; myocardial infarction; superoxide dismutase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Yellon, DM Univ Coll London Hosp, Hatter Inst & Ctr Cardiol, London WC1E 6DB, England Univ Coll London Hosp London England WC1E 6DB 1E 6DB, England
Citazione:
A. Dana et al., "Adenosine A(1) receptor activation induces delayed preconditioning in ratsmediated by manganese superoxide dismutase", CIRCULATION, 101(24), 2000, pp. 2841-2848

Abstract

Background-We have previously described a second window of protection against infarction in rabbits 24 to 72 hours after adenosine A, receptor (A(1)R) activation. In this study, we examined the potential role of the mitochondrial antioxidant manganese superoxide dismutase (Mn-SOD) as a potential end effector in mediating this protection. Methods and Results-Rats were treated with an intravenous bolus of the AIRagonist 2-chloro-N-6-cyclopentyladenosine (CCPA, 75 mu g/kg) or saline vehicle. They were also given a 5 mg/kg IV infusion of a 22-mer phosphorothioate oligodeoxynucleotide (ODN) with sequence antisense to the initiation site of rat Mn-SOD mRNA. Sense ODN and scrambled ODN were used as controls. Twenty-four hours later, hearts were isolated and perfused with buffer at constant pressure and subjected to 35 minutes of regional ischemia and 2 hoursof reperfusion. Treatment with CCPA compared with saline vehicle (control)significantly reduced infarct size, expressed as percentage of myocardium at risk (22.3+/-3.3% versus 42.1+/-3.8%, respectively; P=0.001). This protection was completely abolished by prior treatment with antisense ODN, whichhad no effect on its own. Neither sense ODN nor scrambled ODN had an effect on the CCPA-induced delayed cardioprotection. In separate animals, 24 hours after the same treatment, hearts were assayed for Mn-SOD content and activity. CCPA treatment induced a significant increase in myocardial Mn-SOD content and activity compared with the control condition; this increase was abolished by pretreatment with antisense ODN. Conclusions-This is the first study to show that transient A(1)R activation induces delayed cardioprotection in the rat. These results strongly suggest an important role for mitochondrial Mn-SOD as a potential end effector of this protection.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 17:21:34