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Titolo:
Alterations in myocardial creatinine kinase (CK) and lactate dehydrogenase(LDH) isoenzyme-distribution in a model of left ventricular dysfunction
Autore:
Muders, F; Neubauer, S; Luchner, A; Fredersdorf, S; Ickenstein, G; Riegger, GAJ; Horn, M; Elsner, D;
Indirizzi:
Univ Klinikum, Klin & Poliklin Innere Med 2, D-93042 Regensburg, Germany Univ Klinikum Regensburg Germany D-93042 2, D-93042 Regensburg, Germany Univ Wurzburg, Med Klin, D-97070 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97070 d Klin, D-97070 Wurzburg, Germany
Titolo Testata:
EUROPEAN JOURNAL OF HEART FAILURE
fascicolo: 1, volume: 3, anno: 2001,
pagine: 1 - 5
SICI:
1388-9842(200101)3:1<1:AIMCK(>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENERGY-METABOLISM; RAT HEARTS; SYSTEM; CARDIOMYOPATHY; INFARCTION; FAILURE;
Keywords:
myocardium; creatinine kinase; lactate dehydrogenase; isoenzymes; LV dysfunction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
18
Recensione:
Indirizzi per estratti:
Indirizzo: Muders, F Univ Klinikum, Klin & Poliklin Innere Med 2, D-93042 Regensburg,Germany Univ Klinikum Regensburg Germany D-93042 2 Regensburg, Germany
Citazione:
F. Muders et al., "Alterations in myocardial creatinine kinase (CK) and lactate dehydrogenase(LDH) isoenzyme-distribution in a model of left ventricular dysfunction", EUR J HE FA, 3(1), 2001, pp. 1-5

Abstract

The purpose of the current study was to evaluate myocardial creatinine kinase (CK) and lactate dehydrogenase (LDH) systems in a model of epinephrine-induced cardiomyopathy in rabbits. Eight rabbits received four repetitive epinephrine infusions (300 mg/kg/60 min, i.v.) in 12-day intervals and eightuntreated rabbits served as controls (CTRL). Echocardiography demonstrateda significant deterioration of LV function as well as increased LV-diameter and -mass index in catecholamine-induced cardiomyopathy. Histological examination revealed that repetitive catecholamine infusion resulted in LV fibrous areas with collagenous content and an increase in myocyte width (16.9 /- 0.8 mum vs. CTRL 12.9 +/- 0.9; P < 0.05). LV dysfunction was associatedwith a decreased total LV lactate dehydrogenase activity (LDH; 0.43 +/- 0.03 IU/mg protein vs. CTRL 0.52 +/- 0.04; P < 0.05) whereas total creatininekinase activity was unchanged (CK; 7.30 +/- 0.63 IU/mg protein vs. CTRL 9.20 +/- 0.49, n.s.). Furthermore, myocardial LDH isoenzymes were shifted with a decrease in LDH, and an increase in LDH, and LDH, (LDH,: 84.90 +/- 2.60% vs. CTRL 94.50 +/- 0.40; LDH2: 7.30 +/- 1.20% vs. 1.50 +/- 0.13; LDH3: 5.40 +/- 0.90% vs. 3.20 +/- 0.25; all P < 0.05). Foetal B-CK isoenzymes were significantly increased (CK-MB 5.30 +/- 0.66 vs. 2.20 +/- 0.35%; P < 0.05). The current study demonstrates changes in cardiac energy metabolism including an impaired LDH activity with a shift towards anaerobic isoenzymes as well as a more efficient CK system in a model of catecholamine-induced LV dysfunction. (C) 2001 European Society of Cardiology. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/01/20 alle ore 07:03:24