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Titolo:
P-31 NMR KINETICS STUDY OF CARDIAC METABOLISM UNDER MILD HYPOXIA
Autore:
GOUDEMANT JF; ELST LV; VANHAVERBEKE Y; MULLER RN;
Indirizzi:
UNIV CATHOLIQUE LOUVAIN,EXPTL NMR LAB,BATIMENT LAVOISIER,1 PL LOUIS PASTEUR B-1348 LOUVAIN BELGIUM UNIV MONS,NMR LAB B-7000 MONS BELGIUM
Titolo Testata:
Journal of magnetic resonance. Series B
fascicolo: 3, volume: 106, anno: 1995,
pagine: 212 - 219
SICI:
1064-1866(1995)106:3<212:PNKSOC>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
CREATINE-KINASE REACTION; NUCLEAR MAGNETIC-RESONANCE; SATURATION TRANSFER MEASUREMENTS; FREE-ENERGY CHANGE; RAT-HEART; ATP SYNTHESIS; CONTRACTILE FAILURE; POSTISCHEMIC MYOCARDIUM; OXYGEN-CONSUMPTION; INTACT MYOCARDIUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
48
Recensione:
Indirizzi per estratti:
Citazione:
J.F. Goudemant et al., "P-31 NMR KINETICS STUDY OF CARDIAC METABOLISM UNDER MILD HYPOXIA", Journal of magnetic resonance. Series B, 106(3), 1995, pp. 212-219

Abstract

The effects of mild hypoxia on the metabolic and mechanical functionsof isovolumic perfused rat hearts have been studied. P-31 NMR has been used to follow the metabolite concentrations as well as the intracellular pH. Additionally, the energy transfer through the creatine kinase reaction was estimated by the magnetization-transfer technique. The needs of myofibrillar energy and of mitochondrial ATP production have been assessed through mechanical activity and oxygen-consumption rate. It has been observed that mild hypoxia simultaneously impairs contractile and metabolic functions. The aerobic ATP production is maintainedunder these conditions while anaerobic energy metabolism seems accelerated. The accumulation of some metabolites (ADP and P-i) and the decrease of creatine kinase forward flux (V-for) tend, however, to prove that ATP availability for myofibrils is lowered. The large aerobic energy production observed must therefore be explained by an energy wastage in the mitochondria. In spite of normal ATP concentration, a contractile dysfunction is observed and can be explained by the P-i accumulation, which is known to impair the use of the myofibrillar ATP. Anotherhypothesis supported by the magnetization transfer experiments is thepoor ATP availability resulting from the ATP wastage in the mitochondria and from the inefficient energy transport by the PCr-Cr shuttle. (C) 1995 Academic Press, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 16:16:48