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Titolo:
Role of high-energy phosphate metabolism in hydrogen peroxide-induced cardiac dysfunction
Autore:
Matsumoto, Y; Kaneko, M; Iimuro, M; Fujise, Y; Hayashi, H;
Indirizzi:
Hamamatsu Univ, Sch Med, Dept Internal Med 3, Hamamatsu, Shizuoka 4313124,Japan Hamamatsu Univ Hamamatsu Shizuoka Japan 4313124 u, Shizuoka 4313124,Japan Hamamatsu Univ, Sch Med, Dept Chem, Hamamatsu, Shizuoka 4313124, Japan Hamamatsu Univ Hamamatsu Shizuoka Japan 4313124 , Shizuoka 4313124, Japan Hamamatsu Univ, Sch Med, Photon Med Res Ctr, Hamamatsu, Shizuoka 4313124, Japan Hamamatsu Univ Hamamatsu Shizuoka Japan 4313124 , Shizuoka 4313124, Japan
Titolo Testata:
MOLECULAR AND CELLULAR BIOCHEMISTRY
fascicolo: 1-2, volume: 204, anno: 2000,
pagine: 97 - 106
SICI:
0300-8177(200001)204:1-2<97:ROHPMI>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
OXYGEN-FREE-RADICALS; PERFUSED RAT-HEART; NUCLEAR-MAGNETIC-RESONANCE; INDUCED OXIDATIVE STRESS; GUINEA-PIG; GLYCOLYTIC INHIBITION; REPERFUSION INJURY; ISOLATED RABBIT; K+ CHANNELS; ISCHEMIA;
Keywords:
hydrogen peroxide; high-energy phosphate; nuclear magnetic resonance spectroscopy; glycolytic inhibition; calcium overload;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Matsumoto, Y Hamamatsu Univ, Sch Med, Dept Internal Med 3, 3600 Hando Cho,Hamamatsu, Shizuoka 4313124, Japan Hamamatsu Univ 3600 Hando Cho HamamatsuShizuoka Japan 4313124
Citazione:
Y. Matsumoto et al., "Role of high-energy phosphate metabolism in hydrogen peroxide-induced cardiac dysfunction", MOL C BIOCH, 204(1-2), 2000, pp. 97-106

Abstract

This study was undertaken to clarify the role of high-energy phosphate metabolism in hydrogen peroxide-induced cardiac dysfunction using phosphorus and fluorine nuclear magnetic resonance spectroscopy. The exposure of a Langendorff-perfused heart to hydrogen peroxide (200-400 mu mol/L, 8 min) provoked biphasic contractile dysfunction characterized by a transient depression of left ventricular developed pressure during the administration of hydrogen peroxide and a delayed elevation of left ventricular end-diastolic pressure after the washout of hydrogen peroxide. The initial phase of cardiac dysfunction correlated well with the accumulation of sugar phosphates (r = 0.89, p < 0.01). Furthermore, we demonstrated that glibenclamide, a potent inhibitor of the ATP-sensitive K+ channel, attenuated the initial depressionof developed pressure. On the other hand, the delayed elevation of end-diastolic pressure correlated well with the total ATP depletion (r = 0.96, p <0.01). However, ATP loss was supposed to be a mere result from the increased ATP consumption corresponding to a rise in intracellular free Ca2+ (fromthe control value of 315 +/- 23 nmol/L to 708 +/- 104 after the administration of hydrogen peroxide, p < 0.01), which also paralleled the elevation of end-diastolic pressure. Thus glycolytic inhibition and intracellular Ca2overload are independently responsible for the biphasic contractile dysfunction induced by hydrogen peroxide.

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Documento generato il 02/12/20 alle ore 18:06:30