Influência do exercício físico na remodelação cardíaca induzida pelo ácido retinóico

• Ano de defesa: 2015
• Autor(a) principal: Claro, Renan Floret Turini [UNESP]
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Estadual Paulista (Unesp)
• Palavras-chave em Português: Exercícios físicos; Remodelação ventricular; Ácidos; Vitamina A; Ventricular remodeling
• Link de acesso: http://hdl.handle.net/11449/132030; http://www.athena.biblioteca.unesp.br/exlibris/bd/cathedra/24-11-2015/000854265.pdf

The Retinoic Acid (RA) is a bioactive metabolite of Vitamin A that has its origin in Retinol. The AR can be found in some form of isomers such as 9-cis RA and all-trans-RA (ATRA). They bind to specific receptors (RAR and RXR respectively) and act by activating or repressing the transcription of target genes within the cell nucleus. In the case of ATRA when used as a supplement promotes cardiac remodeling. Physical Exercise (PE) in turn causes cardiac abnormalities classified as physiological and improves function and modify structures to suit the requirements of hemodynamic homeostasis break. PE and RA together can elucidate physiological situations at an early stage. In our protocol we evaluate the influence of exercise on changes in the heart of male Wistar rats treated with RA. For this, we analyzed the effects of the treatments in the heart by echocardiography, the study of the isolated heart, heart weight and histopathology. These analyzes are able to characterize the cardiac remodeling process detecting functional changes, collagen and ventricular hypertrophy elucidating physiological or pathological conditions. Our results showed that animals treated with AR had lower left ventricular end-diastolic diameter adjusted for weight, and low mass index of the left ventricle. Regarding the functional data, the RA association with exercise induced lower systolic pressure, derived positive and negative derivative of pressure. Therefore we can conclude that the association of AR with EF attenuated cardiac hypertrophy and resulted in deleterious effects on systolic and diastolic functions in rats