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European Journal of Heart Failure 2001 3(1):1-5; doi:10.1016/S1388-9842(00)00085-4
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© 2001 European Society of Cardiology

Alterations in myocardial creatinine kinase (CK) and lactate dehydrogenase (LDH) isoenzyme-distribution in a model of left ventricular dysfunction

Frank Mudersa,*, Stefan Neubauerb, Andreas Luchnera, Sabine Fredersdorfa, Guntram Ickensteina, Günter A.J. Rieggera, Michael Hornb and Dietmar Elsnera

a Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum 93042 Regensburg, Germany
b Medizinische Universitätsklinik Würzburg Germany

* Corresponding author. Tel.: +49-941-944-7256; fax: +49-941-944-7213.


  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 eight untreated rabbits served as controls (CTRL). Echocardiography demonstrated a 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 µm vs. CTRL 12.9 ± 0.9; P < 0.05). LV dysfunction was associated with 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 creatinine kinase 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 LDH1 and an increase in LDH2 and LDH3 (LDH1: 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.

Key Words: Myocardium • Creatinine kinase • Lactate dehydrogenase • Isoenzymes • LV dysfunction

Received October 4, 1999; Revised April 20, 2000; Accepted April 28, 2000


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