Infarto do mioc?rdio como modelo de depress?o em ratos: estudo seriado

• Autor(a) principal: C?rtes, Rafael Sonoda
• Data de Publicação: 2012
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da UFRRJ
• Texto Completo: https://tede.ufrrj.br/jspui/handle/jspui/3742
• topic: Infarto do Mioc?rdio; depress?o; serotonina; Myocardial infarction; depression; serotonin; Fisiologia

Cardiovascular diseases, especially myocardial infarction, represent a major challenge to medicine in the world. Recent studies show that patients who have some type of cardiovascular disease are more likely to develop depression. Furthermore, the healthy cardiovascular standpoint, but developed depression are more susceptible to cardiac events. Thus, considering the lack of experimental studies and the bidirectional relationship between depression and MI, we studied the possible effect of heart failure- induced experimental MI by permanent occlusion of the left coronary artery in the default behavior of Wistar rats. For this purpose, we used the Open Field Test, the Test of the Elevated Plus Maze and the Test of Preference for Sucrose, to identify possible signs similar to the psychological anxiety and depression in humans, 3, 14, 35 and 63 days after MI. To evaluate the influence of cardiac autonomic imbalance induced by IM in behavioral changes, we performed a study of heart rate variability. Finally, in order to study the contribution of possible changes in serotonergic transmission in the autonomic and behavioral changes, we gave fluoxetine (serotonin reuptake inhibitor, 10 mg / kg) or vehicle, both by gavage in sham and infarcted groups throughout the protocol. The gene expression of an enzyme precursor of serotonin, tryptophan hydroxylase type 2 (TPH2), was also studied in real time PCR in all groups. The infarcted group showed signs of depression such as reduced exploratory activity and anhedonia, which were almost completely inhibited by fluoxetine. The infarcted group showed changes in cardiac sympathetic tone seen by the increase of low frequency waves in the spectral analysis, compared to sham. Treatment with fluoxetine did not alter this parameter in the infarcted group. TPH2 expression decreased in the infarcted compared to sham and this time, fluoxetine treatment normalized this parameter. Based on data obtained in this study, we conclude that the IM in rats induces signs of depression that are reversed by treatment with fluoxetine and that alterations in cardiac autonomic balance preceding behavioral disturbances may be related to the signs of depression.