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MUSCLE CELL BIOLOGY AND CELL MOTILITY
1Consiglio Nazionale delle Ricerche Institute of Neuroscience, Unit for Neuromuscular Biology and Pathophysiology, Department of Biomedical Sciences, University of Padova, 35100 Padua; 2Istituto di Ricovero e Cura a Conattere Scientifico, Gussago, 25064 Brescia; 3Department of Cardiovascular Pathology, University of Padova, 35100 Padua; and 4Department of Human Anatomy and Physiology and 5Internal Medicine II, S. Bortolo Hospital, 36100 Vicenza, Italy
Submitted 27 March 2003 ; accepted in final form 10 September 2003
Muscle atrophy is a determinant of exercise capacity in heart failure (CHF). Myocyte apoptosis, triggered by tumor necrosis factor-
(TNF-) or its second messenger sphingosine (SPH), is one of the causes of atrophy. Growth hormone (GH) improves hemodynamic and cardiac trophism in several experimental models of CHF, but its effect on skeletal muscle in CHF is not yet clear. We tested the hypothesis that GH can prevent skeletal muscle apoptosis in rats with CHF. CHF was induced by injecting monocrotaline. After 2 wk, 2 groups of rats were treated with GH (0.2 mg·kg–1·day–1 and 1.0 mg·kg–1·day–1) subcutaneously. A third group of controls had saline. After 2 additional weeks, rats were killed. Tibialis anterior cross-sectional area, myosin heavy chain (MHC) composition, and a study on myocyte apoptosis and serum levels of TNF- and SPH were carried out. The number of apoptotic nuclei, muscle atrophy, and serum levels of TNF- and SPH were decreased with GH at high but not at low doses compared with CHF rats. Bcl-2 was increased, whereas activated caspases and bax were decreased. The MHC pattern in GH-treated animals was similar to that of controls. Monocrotaline slowed down both contraction and relaxation but did not affect specific tetanic force, whereas absolute force was decreased. GH treatment restored contraction and relaxation to control values and brought muscle mass and absolute twitch and tetanic tension to normal levels. These findings may provide an insight into the therapeutic strategy of GH given to patients with CHF to improve exercise capacity.
apoptosis; cytokines; myosin heavy chains
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