Mild dystrophic damage in the androgen-sensitive levator ani muscle of the mdx mouse

Mild dystrophic damage in the androgen-sensitive levator ani muscle of the mdx mouse

Autor Souccar, C. Google Scholar
Goncalo, M. D. Google Scholar
Buck, H. D. Google Scholar
lima-Landman, MTR Google Scholar
Lapa, A. J. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Fac Ciencias Med Santa Casa São Paulo
Resumo The time course of muscular dystrophy on the androgen-sensitive levator ani muscle was compared to that of the diaphragm of dystrophic (mdx) mice aged 1-20 months. Muscle growth, isometric contractile properties and caffeine-induced contractures were determined to assess the hormone myotrophic effect, muscle strength and sarcoplasmic reticulum function, respectively, of both control and dystrophic muscles. Histological analysis of mdx muscles showed variable fiber size, centronucleated cells, infiltration of connective tissue, and necrosis which was less severe in the levator am than in the diaphragm muscle. Tetanic tension per unit weight in the mdx levator am was reduced (29%) after aging, while the contraction time remained unchanaed. the tetanic tension of the mdx diaphragm muscle decreased with age from 3 to 20 months (20-64%), and the relaxation time was prolonged after aging (22%). Gonadectomy of young adult mdx mice caused atrophy of the levator am muscle, accelerated muscle wasting, reduced the tetanic force (31%), but it did not affect the contraction time and caffeine responses. the results showed that testosterone does not prevent the progress of muscle disease in the mdx levator am, but androgen withdrawal accelerates muscle wasting suggesting a normonal beneficial effect. (C) 2004 Elsevier B.V. All rights reserved.
Assunto muscle dystrophy
levator ani muscle
contraction properties
caffeine contractures
mdx mouse
Idioma Inglês
Data 2005-01-01
Publicado em Neuromuscular Disorders. Oxford: Pergamon-Elsevier B.V., v. 15, n. 1, p. 48-56, 2005.
ISSN 0960-8966 (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 48-56
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000226567900008

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