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Titolo:
Myocardial creatine kinase kinetics and isoform expression in hearts with severe LV hypertrophy
Autore:
Ye, Y; Wang, CS; Zhang, JY; Cho, YK; Gong, GR; Murakami, Y; Bache, RJ;
Indirizzi:
Univ Minnesota, Sch Med, Dept Med, Div Cardiovasc, Minneapolis, MN 55455 USA Univ Minnesota Minneapolis MN USA 55455 iovasc, Minneapolis, MN 55455 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 1, volume: 281, anno: 2001,
pagine: H376 - H386
SICI:
0363-6135(200107)281:1<H376:MCKKAI>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEFT-VENTRICULAR HYPERTROPHY; CONTRACTILE FAILURE; OXYGEN-CONSUMPTION; PRESSURE-OVERLOAD; CARDIAC-FAILURE; RAT-HEART; ISOENZYMES; TISSUE; INVIVO; ATP;
Keywords:
high-energy phosphates; nuclear magnetic resonance; phosphocreatine; ATP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Zhang, JY Univ Minnesota, Sch Med, Dept Med, Div Cardiovasc, Mayo Mail Code 508,UMHC,420 Delaware St SE, Minneapolis, MN 55455 USA Univ Minnesota Mayo Mail Code 508,UMHC,420 Delaware St SE Minneapolis MN USA 55455
Citazione:
Y. Ye et al., "Myocardial creatine kinase kinetics and isoform expression in hearts with severe LV hypertrophy", AM J P-HEAR, 281(1), 2001, pp. H376-H386

Abstract

Left ventricular (LV) hypertrophy (LVH) results in a fetal shift in myocardial creatine kinase (CK) expression. Because CK plays an important role inintracellular energy production, transport, and utilization, this study was performed to characterize changes in CK expression and CK flux in severe pressure-overload LVH. Ascending aortic banding in 8-wk-old dogs resulted in LVH with a 92% increase in relative LV mass. In LVH hearts, CK-M isoform mRNA was decreased by 40% (P = 0.05) and protein was decreased by 50% (P<0.01), whereas mitochondrial CK protein was decreased by 22% (P<0.05). CK-B isoform mRNA was undetectable in normal hearts but was prominently expressedin LVH (P<0.01); CK-B protein was increased by more than 10-fold in LVH (P<0.01). Despite these changes, total CK activity was normal in LVH. Myocardial CK flux was examined using P-31 magnetic resonance spectroscopy magnetization transfer. The CK forward rate constant was similar in normal and LVHhearts at baseline and did not change in either group during dobutamine treatment. In hearts with LVH, the CK forward flux rate was reduced by similar to 60% (P<0.05) and decreased further during dobutamine. Thus, although pressure-overload LVH caused alterations of expression of both CK mRNA and protein levels, LV performance and oxygen consumption in response to dobutamine were normal. However, myocardial free ADP was increased in LVH hearts. This finding suggests that the CK alterations result in a need for higher ADP levels to maintain ATP synthesis in the hypertrophied heart.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 00:45:38