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Volumn 21, Issue 12, 2002, Pages 1447-1455

Impact of carvedilol on the mitochondrial damage induced by hypoxanthine and xantine oxidase - What role in myocardial ischemia and reperfusion?;Impacto do carvedilol sobre o dano mitocondrial induzido por hipoxantina/xantina oxidase - Que papel na isquemia e reperfusão do miocárdio?

Author keywords

Calcium; Carvedilol; Heart; Mitochondria; Mitochondrial permeability transition; Xantine oxidase

Indexed keywords

CALCIUM; CARVEDILOL; FLUORESCENT DYE; REACTIVE OXYGEN METABOLITE; XANTHINE OXIDASE;

EID: 0036998602     PISSN: 08702551     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article
Times cited : (6)

References (10)
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  • 2
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    • Myocardial ischemia and reperfusion: Direct evidence for free radical generation by electron spin resonance spectroscopy
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  • 3
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    • Oxidative stress during myocardial ischaemia and heart failure
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    • Ferrari, R.1    Agnoletti, L.2    Comini, L.3
  • 4
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    • 2+-dependent pore of possible relevance to reperfusion-induced injury
    • 2+-Dependent Pore of Possible Relevance to Reperfusion-Induced Injury. Biochem J 1990;266:33-9.
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    • Crompton, M.1    Costi, A.2
  • 5
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    • Carvedilol, a new vasodilator and beta adrenoceptor antagonist, is an antioxidant and free radical scavenger
    • Yue TL, Cheng HY, Lysko PG, et al. Carvedilol, a New Vasodilator and Beta Adrenoceptor Antagonist, Is an Antioxidant and Free Radical Scavenger. J Pharmacol Exp Ther 1992;263:92-8.
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    • Yue, T.L.1    Cheng, H.Y.2    Lysko, P.G.3
  • 6
    • 0034652094 scopus 로고    scopus 로고
    • Carvedilol inhibits the exogenous NADH dehydrogenase in rat heart mitochondria
    • Oliveira PJ, Santos DL, Moreno AJM. Carvedilol Inhibits the Exogenous NADH Dehydrogenase in Rat Heart Mitochondria. Arch Biochem Biophys 2000;374:279-85.
    • (2000) Arch Biochem Biophys , vol.374 , pp. 279-285
    • Oliveira, P.J.1    Santos, D.L.2    Moreno, A.J.M.3
  • 7
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    • Opening of the mitochondrial permeability transition pore causes depletion of mitochondrial and cytosolic NAD+ and is a causative event in the death of myocytes in postischemic reperfusion of the heart
    • Di Lisa F, Menabò R, Canton M, Barile M, Bernardi P. Opening of the Mitochondrial Permeability Transition Pore Causes Depletion of Mitochondrial and Cytosolic NAD+ and Is a Causative Event in the Death of Myocytes in Postischemic Reperfusion of the Heart. J Biol Chem 2001;276:2571-5.
    • (2001) J Biol Chem , vol.276 , pp. 2571-2575
    • Di Lisa, F.1    Menabò, R.2    Canton, M.3    Barile, M.4    Bernardi, P.5
  • 8
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    • Inhibitory effect of carvedilol in the high-conductance state of the mitochondrial permeability transition pore
    • Oliveira PJ, Coxito PM, Rolo AP, Santos DL, Palmeira CM, Moreno, AJM. Inhibitory Effect of Carvedilol in the High-Conductance State of the Mitochondrial Permeability Transition Pore. Eur J Pharmacol 2001;412:231-7.
    • (2001) Eur J Pharmacol , vol.412 , pp. 231-237
    • Oliveira, P.J.1    Coxito, P.M.2    Rolo, A.P.3    Santos, D.L.4    Palmeira, C.M.5    Moreno, A.J.M.6
  • 9
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    • Propranolol effects on membrane repolarization time in isolated canine purkinje fibers: Threshold tissue content and the influence of exposure time
    • Pruett JK, Walle T, Walle U. Propranolol Effects on Membrane Repolarization Time in Isolated Canine Purkinje Fibers: Threshold Tissue Content and the Influence of Exposure Time. J Pharmacol Exp Therap 1980;215:539-43.
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    • Pruett, J.K.1    Walle, T.2    Walle, U.3


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.