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Titolo:
Chronic phosphocreatine depletion by the creatine analogue beta-guanidinopropionate is associated with increased mortality and loss of ATP in rats after myocardial infarction
Autore:
Horn, M; Remkes, H; Stromer, H; Dienesch, C; Neubauer, S;
Indirizzi:
Gothenburg Univ, Sahlgrens Hosp, Wallenberg Lab Cardiovasc Res, S-41345 Gothenburg, Sweden Gothenburg Univ Gothenburg Sweden S-41345 es, S-41345 Gothenburg, Sweden Univ Wurzburg, Med Klin, D-8700 Wurzburg, Germany Univ Wurzburg WurzburgGermany D-8700 Med Klin, D-8700 Wurzburg, Germany Univ Oxford, John Radcliffe Hosp, Dept Cardiovasc Med, Oxford OX1 2JD, England Univ Oxford Oxford England OX1 2JD rdiovasc Med, Oxford OX1 2JD, England
Titolo Testata:
CIRCULATION
fascicolo: 15, volume: 104, anno: 2001,
pagine: 1844 - 1849
SICI:
0009-7322(20011009)104:15<1844:CPDBTC>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARDIAC ENERGY-METABOLISM; HEART-FAILURE; DILATED CARDIOMYOPATHY; BIOENERGETIC CONSEQUENCES; KINASE; PERFORMANCE; RESERVE; SPECTROSCOPY; MODEL; ACID;
Keywords:
magnetic resonance imaging; spectroscopy; heart failure; myocardial infarction; creatine kinase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Horn, M Gothenburg Univ, Sahlgrens Hosp, Wallenberg Lab Cardiovasc Res, S-41345 Gothenburg, Sweden Gothenburg Univ Gothenburg Sweden S-41345 345 Gothenburg, Sweden
Citazione:
M. Horn et al., "Chronic phosphocreatine depletion by the creatine analogue beta-guanidinopropionate is associated with increased mortality and loss of ATP in rats after myocardial infarction", CIRCULATION, 104(15), 2001, pp. 1844-1849

Abstract

Background-The failing myocardium is characterized by reductions of phosphocreatine (PCr) and free creatine content and by decreases of energy reserve via creatine kinase (CK), ie, CK reaction velocity (Flux(CK)), It has remained unclear,whether these changes contribute directly to contractile dysfunction. In the present study, myocardial PCr stores in a heart failure model were further depleted by feeding of the PCr analogue beta -guanidinopropionate (Gl?). Functional and metabolic consequences were studied. Methods and Results-Rats were subjected to sham operation or left coronaryartery ligation (MI). Surviving rats were assigned to 4 groups and fed with 0% (n=7, Sham; n=5, MI) or 1% (n=7 Sham+GP, n=8 MI+GP) GP. Two additionalgroups were fed GP for 2 or 4 weeks before MI. After 8 weeks, hearts were isolated and perfused, and left ventricular pressure-volume curves were obtained. High-energy phosphate metabolism was determined with P-31 NMR spectroscopy. After GP feeding or MI, left ventricular pressure-volume curves were depressed by 33% and 32%, respectively, but GP feeding in MI hearts did not further impair mechanical function. Both MI and GP feeding reduced PCr content and Flux(CK), but here, effects were additive. In MI+GP rats, PCr levels and Flux(CK) were reduced by 87% and 94%, respectively. Although ATP levels were maintained in the GP and MI groups, ATP content was reduced by 18% in MI+GP hearts. Furthermore, 24-hour mortality in GP-prefed rats was 100%. Conclusions-Rats with an 87% predepletion of myocardial PCr content cannotsurvive an acute MI. Chronically infarcted hearts subjected to additional PCr depletion cannot maintain ATP homeostasis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/10/20 alle ore 09:16:36