Remodelamento do miocárdio na cardiomiopatia dilatada induzida com doxorrubicina em coelhos

• Ano de defesa: 2014
• Autor(a) principal: Gava, Fábio Nelson [UNESP]
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Estadual Paulista (Unesp)
• Palavras-chave em Português: Coelho; Miocardio - Doenças; Doppler, Ecocardiografia; Imuno-histoquímica; Microscopia eletronica; Apoptose; Immunohistochemistry
• Link de acesso: http://hdl.handle.net/11449/121862

The cardiotoxicity induced by doxorubicin generates myocardial remodeling and systolic dysfunction. The present study evaluated the role of apoptosis and extracellular matrix components (fibronectin and myofibroblasts) in doxorubicin-induced dilated cardiomyopathy in rabbits. Twenty five New Zealand rabbits were used, allocated into two groups (control and treated). The drug was administered for six weeks and Doppler echocardiography was performed before the first and after the last administration. Myocardial remodeling was evaluated by electron microscopy (scanning and transmission) and immunodetection of apoptotic cells, myofibroblasts and fibronectin. Significant reduction in systolic function, increased apoptotic fibers and myofibroblasts were noticed in treated animals, on the left ventricle, interventricular septum and right ventricle. There was a significant negative correlation between the number of damaged mitochondria and apoptotic cells at the left ventricle and interventricular septum with systolic function, showing that the apoptosis by mitochondrial pathway plays a role on the systolic dysfunction during treatment with doxorubicin and the increase in extracellular matrix is not the primary cause of systolic dysfunction induced by doxorubicin