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Titolo:
Functional and energetic consequences of chronic myocardial creatine depletion by beta-guanidinopropionate in perfused hearts and in intact rats
Autore:
Neubauer, S; Hu, K; Horn, M; Remkes, H; Hoffmann, KD; Schmidt, C; Schmidt, TJ; Schnackerz, K; Ertl, G;
Indirizzi:
Univ Wurzburg, Med Klin, Theodor Boveri Inst Biowissensch Physiol Chem 1, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 Chem 1, D-97080 Wurzburg, Germany Univ Heidelberg, Med Klin Mannheim, Heidelberg, Germany Univ Heidelberg Heidelberg Germany d Klin Mannheim, Heidelberg, Germany
Titolo Testata:
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
fascicolo: 10, volume: 31, anno: 1999,
pagine: 1845 - 1855
SICI:
0022-2828(199910)31:10<1845:FAECOC>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
MECHANICAL FUNCTION; KINASE REACTION; INFARCTION; METABOLISM; ANALOG; ENDOTHELIN-1; ADAPTATION; DEFICIENCY; TURNOVER; FAILURE;
Keywords:
P-31-NMR spectroscopy; cardiac energy metabolism; heart failure; total creatine content; creatine kinase reaction velocity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Neubauer, S Univ Wurzburg, Med Klin, Theodor Boveri Inst Biowissensch Physiol Chem 1, Josef Schneider Str 2, D-97080 Wurzburg, Germany Univ Wurzburg Josef Schneider Str 2 Wurzburg Germany D-97080
Citazione:
S. Neubauer et al., "Functional and energetic consequences of chronic myocardial creatine depletion by beta-guanidinopropionate in perfused hearts and in intact rats", J MOL CEL C, 31(10), 1999, pp. 1845-1855

Abstract

Oral feeding with the creatine analogue beta-guanidinopropionate (beta-GP)reduces myocardial phosphocreatine and creatine concentrations by about 80%; in vitro, this is accompanied by reduced contractile performance. We hypothesized, thus, that beta-GP feeding leads to hemodynamic changes in vivo characteristic of heart failure. beta-GP was fed to Wistar rats for up to 8weeks. In isolated hearts, function was measured isovolumically, myocardial energetics were followed with P-31-NMR spectroscopy. In vivo hemodynamicswere measured with Millar-Tip-catheters and an electromagnetic flow probe.beta-GP feeding did not alter heart weight, In vitro, diastolic pressure-volume curves indicated structural left ventricular dilatation, and a 36% reduction of left ventricular developed pressure was found; phosphocreatine was reduced by similar to 80%, ATP unchanged and creatine kinase reaction velocity P-31-MR saturation transfer) decreased by similar to 90%. The total creatine pool thigh-pressure liquid chromatography) was reduced by up to similar to 70%. In contrast to in vitro findings, in vivo cardiac hemodynamics (including left ventricular developed pressure, dP/dt(max), cardiac output and peripheral vascular resistance) at rest and during acute volume loading showed no alterations after beta-GP feeding, The only functional impairment observed in vivo was a 14% reduction of maximum left ventricular developed pressure during brief aortic occlusion. In the intact rat, cardiac and/or humoral compensatory mechanisms are sufficient to maintain normal hemodynamics in spite of a 90% reduction of creatine kinase reaction velocity. However, chronic beta-GP feeding leads to structural left ventricular dilatation. (C) 1999 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 10:33:22