Repercussão da terapia combinada de carvedilol e fotobiomodulação no remodelamento cardíaco em ratos infartados

• Autor(a) principal: Carlos, Fernando Pereira
• Data de Publicação: 2017
• Tipo de documento: Tese
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da Uninove
• Texto Completo: http://bibliotecatede.uninove.br/handle/tede/2700
• topic: remodelamento cardíaco; insuficiência cardíaca; fotobiomodulação; laser de baixa intensidade; carvedilol; desempenho físico; cardiac remodeling; heat failure; photobiomodulation; low level laser therapy; carvedilol; CIENCIAS DA SAUDE

Heart failure is an important cause of morbidity and mortality worldwide and responsible for the high number of hospitalizations. Activation of neurohormonal mechanisms and persistent inflammation become deleterious in the long term by stimulating ventricular remodeling, overcoming further deterioration to an already weakened heart. Low level laser therapy (LLLT) is a promising tool to attenuate cardiac remodeling resulting from myocardial infarction (MI). It is mentioned that previous studies of the literature have pointed to the isolated repercussion of LLLT, in which its action added or compared to standard pharmacological therapy of heart failure was not investigated. Thus, the objective was to analyze the effect of Carvedilol and LLLT in post-infarct cardiac remodeling in rats. Female wistarrats were randomized into five experimental groups: SHAM; untreated infarct (IM); infarcted + caverdilol (IMC); infarcted + LBI (IML); infarcted + LBI + carvedilol (IMCL). The LLLT (λ 830 nm, 100 mW, 200 s, 20 J) was applied transthoracic three times weekly between the costal arcs. Animals receiving caverdilol received daily doses of 1mg/100g. Biometric data were collected after sacrifice, in which the heart and left ventricle (LV) and the pulmonary water content (H2O). The hemodynamic parameters of the LV were evaluated at baseline with intra-VE implantation of a MILLAR catheter and flow transducer positioned in the ascending portion of the aorta. The following variables were obtained: systolic pressure (PS); Final diastolic pressure (PD2); derivative of positive pressure (+ dP / dt) and negative (-dP / dt); Cardiac output; Systolic work. Only animals with infarctions ≥37% were included in the study. nflammatory markers (interleukin 1β, interleukin-6, interleukin-10, and tumor necrosis factor alpha) were analyzed by the ELISA method. Only animals with infarctions ≥37% were included in the study. Data are expressed as mean ± standard error of the mean and ANOVA (post-hoc: Bonferroni).LLLT did not affect the heart weight / body weight ratio between groups, but combined with carvedilol attenuated the increase in LV weight / body weight ratio induced by MI. H2O was attenuated by all therapies. PS was significantly reduced in all infarcted groups. The increase in post-MI PD2 was reduced with all treatments. Both + dP / dt and -dP / dt were reduced with MI and unaffected by therapies. The CD was similar between groups. The proinflammatory cytokines were modulated by LLLT and when combined with carvedilol.Our results are the first to demonstrate the effects of LLLT combined with carvedilol and what considerations of physical performance, cardiopulmonary biometry and morphofunctionality appear to be similar. However, we observed the anti-inflammatory effect of LBI to be more evident than pharmacological therapy. In addition, the combination of therapies resulted in attenuation of myocardial hypertrophy and improvement of FAC.