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1 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET; Departments of 3 Biochemistry and Molecular Biology and 4 Medicine, University of Leeds, Leeds LS2 9JT, United Kingdom; and 2 Michael Reese Hospital and Medical Center, Chicago, Illinois 60616-3990
Myocyte-specific necrosis in
the heart and soleus muscle of adult male Wistar rats was investigated
in response to a single subcutaneous injection of the anabolic
2-adrenergic receptor agonist clenbuterol. Necrosis was
immunohistochemically detected by administration of a myosin antibody
1 h before the clenbuterol challenge and quantified by using image
analysis. Clenbuterol-induced myocyte necrosis occurred against a
background of zero damage in control muscles. In the heart, the
clenbuterol-induced necrosis was not uniform, being more abundant in
the left subendocardium and peaking 2.4 mm from the apex. After
position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and
sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was
found to be 1.0 ± 0.2%. In response to the same parameters
(i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte
necrosis was 4.4 ± 0.8% in the soleus. These data show
significant myocyte-specific necrosis in the heart and skeletal muscle
of the rat. Such irreversible damage in the heart suggests that
clenbuterol may be damaging to long-term health.
anabolic adrenergic agonist; cardiomyocytes; sympathomimetic; necrosis; immunohistochemistry; -adrenergic antagonists
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