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Titolo:
Protective effects of FK409, a novel nitric oxide donor, against postischemic myocardial dysfunction in guinea-pig hearts
Autore:
Cao, YT; Hotta, Y; Shioi, K; Nagata, Y; Kawai, N; Ishikawa, N;
Indirizzi:
Aichi Med Univ, Sch Med, Dept Pharmacol, Nagakute, Aichi 4801195, Japan Aichi Med Univ Nagakute Aichi Japan 4801195 agakute, Aichi 4801195, Japan Aichi Med Univ, Sch Med, Dept Surg 2, Nagakute, Aichi 4801195, Japan AichiMed Univ Nagakute Aichi Japan 4801195 agakute, Aichi 4801195, Japan Aichi Med Univ, Sch Med, Dept Anat, Nagakute, Aichi 4801195, Japan Aichi Med Univ Nagakute Aichi Japan 4801195 agakute, Aichi 4801195, Japan
Titolo Testata:
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
fascicolo: 4, volume: 38, anno: 2001,
pagine: 593 - 605
SICI:
0160-2446(200110)38:4<593:PEOFAN>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIA-REPERFUSION INJURY; NUCLEAR-MAGNETIC-RESONANCE; OXYGEN-FREE RADICALS; INTRACELLULAR PH; CARDIAC MITOCHONDRIA; FAILING MYOCARDIUM; SYNTHASE; CALCIUM; PEROXYNITRITE; DIHYDROOUABAIN;
Keywords:
nitric oxide electrode; Ca2+ fluorometry; P-31 nuclear magnetic resonance; ischemia-reperfusion; left ventricular developed pressure; St. Thomas' Hospital solution;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Hotta, Y Aichi Med Univ, Sch Med, Dept Pharmacol, 21 Yazakoaza Karimata, Nagakute, Aichi 4801195, Japan Aichi Med Univ 21 Yazakoaza Karimata NagakuteAichi Japan 4801195
Citazione:
Y.T. Cao et al., "Protective effects of FK409, a novel nitric oxide donor, against postischemic myocardial dysfunction in guinea-pig hearts", J CARDIO PH, 38(4), 2001, pp. 593-605

Abstract

Effects of FK409 were investigated in perfused guinea-pig Langendorff hearts subjected to ischemia and reperfusion. Nitric oxide electrode, fluorometry, and P-31 nuclear magnetic resonance imaging were used to monitor changes in cellular high-phosphorous energy and nitric oxide and Ca2+, content inthe heart together with simultaneous recordings of left ventricular developed pressure. After cardioplegic arrest with St. Thomas' Hospital solution,normothermic (37 degreesC) global ischemia was induced for 40 min, and hearts were reperfused for 40 min. FK409 at 10(-8) M, which has a minimum inotropic effect on nonischemic hearts, was added to the cardioplegic solution. Treatment with FK409 reduced left ventricular developed pressure during and after ischemia and improved postischemic recovery of left ventricular developed pressure from 55.4% at 40 min of reperfusion in FK409-free hearts upto 80.4% in hearts treated with FK409 (p < 0.01). Flow rate at 1.5 min after treatment with the cardioplegic solution was 27.7 ml/min in hearts treated with FK409 compared with 21.2 ml/min in drug-free hearts (p < 0.01). Treatment with FK409 significantly effected preservation of tissue level of beta -adenosine triphosphate at the end of ischemia or reperfusion. During ischemia, arrested with the cardioplegic solution, intracellular Cat, accumulation and nitric oxide release were reduced. At the end of ischemia in FK409-treated hearts, nitric oxide release was 86% greater than in drug-free hearts without reference to the Ca2+ concentration. In cardiac surgery, normothermic arrested hearts are subject to damage by oxygen free radicals in reperfusion injury. Therefore, nitric oxide exogenously supplied by FK409 wasresponsible for the cardioprotective action, presumably by acting directlyas an oxygen radical scavenger during reperfusion. A specific nitric oxidedonor, like FK409, may have therapeutic use as a nitric oxide-mediated vasorelaxant and additional protective action for reperfusion-injury hearts.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 09:47:25