Caracterização morfológica, bioquímica e molecular do músculo esquelético sóleo de ratos espontaneamente hipertensos com insuficiência cardíaca
Carregando...
Data
2010-02-26
Autores
Damatto, Ricardo Luiz [UNESP]
Título da Revista
ISSN da Revista
Título de Volume
Editor
Universidade Estadual Paulista (Unesp)
Resumo
A insuficiência cardíaca (IC) caracteriza-se por redução da tolerância aos exercícios com a ocorrência precoce de fadiga e dispnéia. Além de disfunção cardíaca e pulmonar, anormalidades intrínsicas da musculatura esquelética têm sido responsabilizadas pela intolerância aos esforços físicos. Em músculos periféricos e respiratórios, frequentemente são observadas atrofia e modificação nas isoformas das cadeias pesadas de miosina (MyHC) na IC. Os mecanismos e vias intracelulares de sinalização responsáveis por essas alterações ainda não estão completamente definidos. Em modelos experimentais de IC induzida por estenose aórtica ou infarto do miocárdio, verificamos que alterações na expressão dos fatores de regulação miogênica e da via miostatina/folistatina podem modular o trofismo muscular e a composição das MyHCs. Um dos modelos experimentais muito utilizados para o estudo da IC é o rato espontaneamente hipertenso (SHR). Estes animais apresentam, precocemente, hipertensão arterial e hipertrofia ventricular esquerda e, em idade avançada, desenvolvem IC. Não identificamos estudos que avaliaram o comprometimento da musculatura esquelética de SHR com IC. O objetivo deste estudo foi caracterizar as alterações da musculatura esquelética de SHR com IC por meio de avaliação da morfologia, das isoformas das cadeias pesadas de miosina e da expressão gênica e protéica dos fatores de regulação miogênica e da via miostatina/folistatina. A partir de 18 meses de idade, ratos espontaneamente hipertensos foram avaliados duas vezes por semana à procura de evidências clínicas de IC como taquipnéia, perda de peso e apatia. Após a detecção de IC, os animais foram submetidos a ecocardiograma transtorácico para a confirmação de disfunção ventricular e eutanasiados. No momento da eutanásia, foram...
Heart failure (HF) is characterized by limited exercise tolerance due to increased muscle fatigue and impaired endurance. Besides cardiac and pulmonary dysfunction, intrinsic skeletal muscle abnormalities have been shown to be involved on reduced exercise tolerance. muscle mass loss and a shift in myosin heavy chain (MyHC) isoforms have been frequently observed in peripheral and respiratory skeletal muscles during HF. The pathophysiological mechanisms and intracellular pathways responsible for muscle changes are not completely defined. We observed that myogenic regulatory factors expression and myostation/follistatin pathway modulate muscle trophism and MyHC isoforms in experimental aortic stenosis- and myocardial infarction-induced HF. The spontaneously hypertensive rat (SHR) is often used in HF studies. These rats develop systemic arterial hypertension and left ventricular hypertrophy early and HF at 18-22 month-age approximately. To the best of our knowledgement, there is not study on skeletal muscle evaluation in SHR with HF. The aim of this study was to characterize skeletal myopathy of SHR with HF by evaluating soleus muscle morphology, MyHC isoforms, and gene and protein expression of myogenic regulatory factors, myostatin, and follistatin. Eighteen month-old spontaneously hypertensive rats were evaluated twice a week to identify HF clinical features such as taquipnea, weight loss, and apathy. After detecting HF, rats were subjected to transthoracic echocardiogram. During euthanasia, we evaluated pathological evidences of HF such as pleuropericardial effusion, ascites, left atrial thrombi, right ventricular hypertrophy, and lung congestion. Agematched Wistar-Kyoto rats used as controls. Soleus morphology was analyzed in haematoxyin and eosin and picro-sirius red stained sections, and MyHC isoforms were evaluated by protein... (Complete abstract click electronic access below)
Heart failure (HF) is characterized by limited exercise tolerance due to increased muscle fatigue and impaired endurance. Besides cardiac and pulmonary dysfunction, intrinsic skeletal muscle abnormalities have been shown to be involved on reduced exercise tolerance. muscle mass loss and a shift in myosin heavy chain (MyHC) isoforms have been frequently observed in peripheral and respiratory skeletal muscles during HF. The pathophysiological mechanisms and intracellular pathways responsible for muscle changes are not completely defined. We observed that myogenic regulatory factors expression and myostation/follistatin pathway modulate muscle trophism and MyHC isoforms in experimental aortic stenosis- and myocardial infarction-induced HF. The spontaneously hypertensive rat (SHR) is often used in HF studies. These rats develop systemic arterial hypertension and left ventricular hypertrophy early and HF at 18-22 month-age approximately. To the best of our knowledgement, there is not study on skeletal muscle evaluation in SHR with HF. The aim of this study was to characterize skeletal myopathy of SHR with HF by evaluating soleus muscle morphology, MyHC isoforms, and gene and protein expression of myogenic regulatory factors, myostatin, and follistatin. Eighteen month-old spontaneously hypertensive rats were evaluated twice a week to identify HF clinical features such as taquipnea, weight loss, and apathy. After detecting HF, rats were subjected to transthoracic echocardiogram. During euthanasia, we evaluated pathological evidences of HF such as pleuropericardial effusion, ascites, left atrial thrombi, right ventricular hypertrophy, and lung congestion. Agematched Wistar-Kyoto rats used as controls. Soleus morphology was analyzed in haematoxyin and eosin and picro-sirius red stained sections, and MyHC isoforms were evaluated by protein... (Complete abstract click electronic access below)
Descrição
Palavras-chave
Hipertensão, Insuficiencia cardiaca, Hipertensão arterial, Cardiac and pulmonary dysfunction, Changes of skeletal muscle
Como citar
DAMATTO, Ricardo Luiz. Caracterização morfológica, bioquímica e molecular do músculo esquelético sóleo de ratos espontaneamente hipertensos com insuficiência cardíaca. 2010. 60 f. Dissertação (mestrado) - Universidade Estadual Paulista, Faculdade de Medicina de Botucatu, 2010.