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

The purpose of the current study was to evaluate myocardial creatinine kina se (CK) and lactate dehydrogenase (LDH) systems in a model of epinephrine-i nduced cardiomyopathy in rabbits. Eight rabbits received four repetitive ep inephrine 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 exam ination revealed that repetitive catecholamine infusion resulted in LV fibr ous 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 associated with a decreased total LV lactate dehydrogenase activity (LDH; 0.43 +/- 0.0 3 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 9.2 0 +/- 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: 5.4 0 +/- 0.90% vs. 3.20 +/- 0.25; all P < 0.05). Foetal B-CK isoenzymes were s ignificantly increased (CK-MB 5.30 +/- 0.66 vs. 2.20 +/- 0.35%; P < 0.05). The current study demonstrates changes in cardiac energy metabolism includi ng an impaired LDH activity with a shift towards anaerobic isoenzymes as we ll as a more efficient CK system in a model of catecholamine-induced LV dys function. (C) 2001 European Society of Cardiology. All rights reserved.