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| Author(s): |
Aline Villa Nova Bacurau
Total Authors: 1
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| Document type: | Master's Dissertation |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Escola de Educação Física e Esportes (EEFE/BT) |
| Defense date: | 2007-03-16 |
| Examining board members: |
Patricia Chakur Brum;
Anselmo Sigari Moriscot;
Paulo Rizzo Ramires
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| Advisor: | Patricia Chakur Brum |
| Abstract | |
Heart failure (HF) is a clinical syndrome with high incidence and bad prognostic, characterized by fatigue, dyspnea, and increased intolerance to exercise. These changes are not only related to the cardiovascular tissue, but are at least in part, consequence of morphofunctional alterations in skeletal muscles. To the present study it was used mice lacking both ?2A/?2C AR subtypes (KO) which develop cardiomyopathy induced by sympathetic hyperactivity, associated to clinical signals of HF and 50% of mortality at seven months of age. The aim of the present study was characterize the phenotype of skeletal muscle by functional and morphological evaluations in KO before (three months of age) and during the HF progression (five and seven months of age). Skeletal muscle alterations due HF were observed only at seven months of age. The alterations were characterized by vascular rarefaction, muscular atrophy, increase in glycolitic fibers percentage and reduction of maximal activity of citrate synthase and contributed with early fatigue observed in this model, and consequently, exercise intolerance. The results of present study suggest that KO mice present morphofunctional changes in skeletal muscles in a similarly to others models of HF and in patients that have this syndrome. Therefore, consisting in an excellent experimental model to future studies related to therapeutic strategies to minimize the skeletal muscle changes due HF (AU) | |