© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Skeletal muscle myosin heavy chain expression in rats with monocrotaline-induced cardiac hypertrophy and failure. Relation to blood flow and degree of muscle atrophy
aFirst Division of Internal Medicine, Venice City Hospital, Castello, 30100 Venice, Italy
bCentro di Fisiopatologia Cardiovascolare, Fondazione Maugeri, Gussago, Brescia, Italy
cCNR Unit for Muscle Biology and Pathophysiology, University of Padua, Padua, Italy
* Corresponding author. Tel.: +39 (41) 529 4361; Fax: +39 (41) 529 4653; E-mail: ldl@civ.bio.unipd.it
Background: In congestive heart failure (CHF) the skeletal muscle of the lower limbs develops a myopathy characterised by atrophy and shift from the slow to the fast type fibres. The mechanisms responsible for these changes are not clear yet. Objectives: We investigated the influence of blood flow and degree of muscle atrophy on the myosin heavy chains (MHC) composition of the soleus and extensor digitorum longus (EDL) of rats with right ventricle hypertrophy and failure. Methods: CHF was induced in 16 rats by injecting 30 mg/kg monocrotaline. Eight animals had the same dose of monocrotaline but resulting in compensated right ventricle hypertrophy. Two age- and diet-matched groups of control animals (nine and five respectively) were also studied. The relative percentage of MHC1 (slow isoform), MHC2a (fast oxidative) and MHC2b (fast glycolytic) was determined by densitometric scan after electrophoretic separation. The relative weights of soleus and EDL (muscle weight/body weight) were taken as an index of muscle atrophy. Skeletal muscle blood flow was measured by injecting fluorescent microspheres. Results: CHF and Control (Con) rats showed similar degree of atrophy both in soleus (0.40±0.06 vs. 0.44±0.06 p=NS), and EDL (0.47±0.04 vs. 0.45±0.02, p=0.09). In CHF rats these two muscles showed a statistically significant MHCs redistribution toward the fast type isozymes. In fact in EDL of CHF rats MHC2a was 30.5±6.1% vs. 35.8±8.6% of the Con (p<0.05). MHC2b was however higher (68.5±6.6% vs. 61.0±9.6%, p=0.017). In the soleus of CHF rats MHC1 was decreased (87.6±3.4% vs. 91.9±5.2%, p=0.02), while MHC2a was increased (12.04±3.5% vs. 7.9±5.2%; p=0.028). Similar changes were not found in the muscles of the compensated hypertrophy animals. No correlation was found between MHC pattern and the relative muscle weight in the CHF animals. Soleus blood flow in CHF rats was significantly lower than that of Con (0.11±0.03 ml/min/g vs. 0.22±0.03 p<0.05), while no differences were found in EDL (0.06±0.02 ml/min/g vs. 0.08±0.02, p=NS). Conclusions: In rats with CHF a skeletal muscle myopathy characterised by a shift of the MHCs toward the fast type isoforms occurs. The magnitude of the shift correlates neither with the degree of atrophy, nor with the skeletal muscle blood flow, suggesting that these two factors do not play a pivotal role in the pathogenesis of the myopathy.
KEYWORDS Heart failure; Myosin heavy chains; Skeletal muscle; Monocrotaline
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