Submitted by Jorge Silva (jorgelmsilva@ufrrj.br) on 2017-11-09T18:21:47Z No. of bitstreams: 1 2016 - Rafael Sonoda C?rtes.pdf: 1476755 bytes, checksum: 8d385f19ac5f844e345d9c74ea4ca89f (MD5) / Made available in DSpace on 2017-11-09T18:21:47Z (GMT). No. of bitstreams: 1 2016 - Rafael Sonoda C?rtes.pdf: 1476755 bytes, checksum: 8d385f19ac5f844e345d9c74ea4ca89f (MD5) Previous issue date: 2016-07-29 / CAPES / Myocardial infarction (MI) is the most prevalent nowadays syndrome. Similarly impressive, depression has caused many damages to health and the global economy. Epidemiologically, these different clinical conditions have a bidirectional relationship. Several studies in rats, in recent years, associated the emergence of analog signals depression post pathophysiological IM changes, among which the activation of pro-inflammatory factors and the activation of the hypothalamic-pituitary-adrenal endocrine axis (HPA). The objective of this study was: to study, in different rat groups, a short-term protocol, four days and a long, twenty-five days, the above features, besides elucidating the involvement of brain-derived neurotrophic factor (BDNF ) and hippocampal neurogenesis in the onset of depression induced experimental IM by ki-67 protein, cell proliferation marker. For this purpose, male Wistar rats (200-250 g) were subjected to IM through ligation of the left coronary artery and underwent preference for sucrose test and the open field test. They were measured: cardiac TNF-?, plasma and hypothalamic concentrations of TNF-? and IL-1?. In endocrine handle, plasma concentrations of adrenocorticotropic hormone (ACTH) and corticosterone and hypothalamic levels of corticotropin releasing hormone (CRH). Finally, we measured plasma concentrations of BDNF to the association with the neurogenesis of the hippocampus, an important region in the pathophysiology of depression. In the long protocol, infarcted animals showed similar signs of depression compared to those operated fake animals. Concomitantly, showed elevated levels of TNF-? and IL-1?, CRH, ACTH and corticosterone plasma levels and reduced BDNF, suggesting decreased proliferation of granule cells in the hippocampus and hence the emergence of depression in response to MI. Although further studies are required, it is believed that this study has translational impact serving experimental basis for the development of more effective future pharmacologic strategies to better quality and life expectancy of patients with myocardial infarction. / O infarto do mioc?rdio (IM) ? a s?ndrome de maior preval?ncia nos dias atuais. Semelhantemente impactante, a depress?o tem causado diversos preju?zos ? sa?de e a economia mundial. Epidemiologicamente, essas diferentes condi??es cl?nicas possuem uma rela??o bidirecional. Diversos estudos em ratos, nos ?ltimos anos, associam o surgimento de sinais an?logos a depress?o a altera??es fisiopatol?gicas p?s IM, dentre as quais a ativa??o de fatores pr?-inflamat?rios e a hiperativa??o do eixo end?crino hipot?lamo-hip?fise-adrenal (HPA). O objetivo deste trabalho foi: estudar, em grupos distintos de ratos, num protocolo a curto prazo, de quatro dias e num longo, de vinte e cinco dias, as caracter?sticas supracitadas, al?m de elucidar a participa??o do fator neurotr?fico derivado do c?rebro (BDNF) e da neurog?nese hipocampal no surgimento da depress?o induzida por IM experimental, atrav?s da prote?na ki-67, marcador de prolifera??o celular. Para tanto, ratos Wistar machos (200-250g) foram submetidos ao IM atrav?s da ligadura da art?ria coron?ria esquerda e submetidos ao teste de prefer?ncia pela sacarose, teste do nado for?ado e ao teste do campo aberto. Foram mensurados: os n?veis card?acos de TNF-? e as concentra??es plasm?ticas e hipotal?micas de TNF-? e IL-1?. Na al?a end?crina, as concentra??es plasm?ticas de horm?nio adrenocorticotr?fico (ACTH) e de corticosterona e os n?veis hipotal?micos de horm?nio liberador de corticotrofina (CRH). Por fim, foi mensurada as concentra??es plasm?ticas de BDNF para a associa??o com a neurog?nese do hipocampo, regi?o importante na fisiopatologia da depress?o. No protocolo longo, os animais infartados apresentaram sinais an?logos a depress?o em compara??o aos animais falso operados. Concomitantemente, apresentaram n?veis elevados de TNF-? e IL-1?, de CRH, ACTH e corticosterona e concentra??es plasm?ticas diminu?das de BDNF, sugerindo diminui??o da prolifera??o de c?lulas granulares no hipocampo e, consequentemente, o surgimento da depress?o em resposta ao IM. Embora sejam necess?rios mais estudos, acredita-se que este trabalho tenha impacto translacional, servindo de base experimental para o desenvolvimento de futuras estrat?gias farmacol?gicas mais eficazes para melhor qualidade e expectativa de vida de pacientes com infarto do mioc?rdio. Palavras chave: Infarto, citocinas, depress?o