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1 Unit for Neuromuscular Biology and Pathophysiology, Department of Biomedical Sciences, University of Padova, CNR Institute of Neuroscience, Padova, Italy
2 IRCCS, Gussago (BS), Italy
3 Department of Cardiovascular Pathology, University of Padova, Padova, Italy
4 Department of Human Anatomy and Physiology, University of Padova, Padova, Italy
5 Internal Medicine II, S. Bortolo Hospital, Vicenza, Italy
* To whom correspondence should be addressed. E-mail: ldl{at}bio.unipd.it.
Muscle atrophy is a determinant of exercise capacity in heart failure (CHF). Myocyte apoptosis, triggered by tumor necrosis factor-
(TNF[[alpha]) or its second messenger sphingosine (SPH) is one of the causes of atrophy. Growth hormone (GH) improves haemodynamic and cardiac trophism in several experimental models of CHF, but its effect on skeletal muscle in CHF is not clear yet. We tested the hypothesis that GH can prevent skeletal muscle apoptosis in rats with CHF. CHF was induced by injecting monocrotaline. After two weeks, two groups of rats were treated with GH: 0.2 mg/kg/die and 1.0 mg/kg/die 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[[alpha]) and SPH were carried out. The number of apoptotic nuclei, muscle atrophy and serum levels of TNF[[alpha] and SPH were decreased with GH at high but not at low doses compared to CHF rats. Bcl-2 was increased while activated caspases and bax were decreased. The MHC pattern in GH-treated animals was similar to that of controls. Monocrotaline slows down both contraction and relaxation, but does not affect specific tetanic force, while absolute force is decreased. GH treatment restores contraction and relaxation to control values and brought to normal muscle mass and absolute twitch and tetanic tension. These findings may provide an insight into the therapeutic strategy of GH given to patients with CHF in order to improve exercise capacity.
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