Influência do treinamento físico aeróbio associado à terapia com células-tronco mesenquimais na morfologia e função do ventrículo direito de ratos com infarto do miocárdio induzido no ventrículo esquerdo

• Ano de defesa: 2014
• Autor(a) principal: Belfort, Felipe Gomes
• Orientador(a): Natali, Antônio José
• Banca de defesa: Lunz, Wellington , Carneiro Júnior, Miguel Araujo
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Viçosa
• Programa de Pós-Graduação: Mestrado em Educação Física
• Departamento: Aspectos sócio-culturais do movimento humano; Aspectos biodinâmicos do movimento humano
• País: BR
• Palavras-chave em Português: Exercícios físicos; Células-tronco; Infarto do miocárdio; Coração - ventrículos
• Palavras-chave em Inglês: Physical exercise; Stem cells; Myocardial infarction; Heart - ventricles
• Área do conhecimento CNPq: CNPQ::CIENCIAS DA SAUDE::EDUCACAO FISICA
• Link de acesso: http://locus.ufv.br/handle/123456789/3500

The aim of this study was to investigate the influence of aerobic exercise training associated with mesenchymal stem cells (MSCs) therapy in the morphology and function of the right ventricle (RV) of rats with infarct (IM) in the left ventricle (LV). Ninety six Wistar male rat (age: 30 days; body weight: 146g ± 10 g) were randomly divided into experimental groups of 16 animals each: sedentary simulated surgery (SED SHAM); sedentary infarcted (SED IM); sedentary infarcted and treated with MSCs (SED IM CT); exercised simulated surgery (EX SHAM); exercised infarcted (EX IM); and exercised infarcted and treated with MSCs (EX IM CT). At the onset and at the end of experimental period all animals were submitted an incremental exercise test to determine the total exercise time until fatigue (TTF). The maximum running speed (MRS) achieved in this test was used to determine the intensity of the exercise training. Twenty four hours after IM in LV and infusion of the MSCs or simulated operation animals from exercised groups started the running training program with incremental load on a motor- driven treadmill (final velocity: 60 % of MRS, 60min/day, 0o inclination, 5 days/week) that lasted for 12 weeks. The animals from sedentary groups remained in their cages for the same period. At the end of the experimental period, eight animals from each group were used for histological and echocardiographic (ECO) evaluations. Right ventricular myocytes from the remained animals of each group were enzymatically isolated and were for measuring cellular morphology, contractility and intracellular global calcium transient [Ca2+]i (stimulation frequency of 1Hz at a room temperature of ~ 25oC). The results showed that exercised animals presented higher TTF than sedentary ones (p < 0,05). The extension of IM was on average 30.40% and it increased heart weight, ventricular weight and ventricular to body weight ratio (p < 0.05). No effects of IM on the absolute and relative RV weights were observed. IM decreased RV function (TAPSE: SED IM = 0,54 ± 0,16 cm vs SED SHAM = 1,40 ± 0,21cm) (p &#8804; 0,05), however, no effects of the IM were detected on the RV morphological and structural properties as well as on myocyte morphology (p > 0.05). Myocardial infarction increased the amplitude of cell contraction and of the [Ca2+]i transient (p < 0,05) but reduced both the times to peak and to 50% decay of the [Ca2+]i transient (p < 0.05). Cell therapy resulted in a reduction of IM extension (15,00%) and attenuated the decrease in the RV function (TAPSE: SED IM CT = 1,28 ± 0,17cm vs SED IM = 0,54 ± 0,16 cm) (p < 0,05). However, no effects of cell therapy were found on heart weight, absolute and relative ventricular weights, absolute and relative RV weights, and on RV cell morphology (p > 0,05). Cellular therapy reduced (p< 0,05) the amplitude and time to peak of cell contraction, decreased the amplitude of the [Ca2+]i transient and increased the times to peak and to 50% decay of the [Ca2+]i transient. Exercise training reduced the IM extension (21.33%), but it did not affect heart weight, ventricular weight, ventricular to body weight ratio, absolute and relative RV weight, RV structural morphology as well as cell morphology (p > 0,05). Exercise training improved RV function (TAPSE: EX IM = 1,47 ± 0,17cm vs SED IM = 0,54 ± 0,16 cm), reduced the amplitude of cell contraction and the time to 50% relaxation (p < 0,05) and increased the time to peak of the [Ca2+]i transient (p < 0,05). The combination of treatments (EX + MSCs) had no effects on IM extension, RV function, heart weight, absolute and relative ventricular weights, absolute and relative RV weights, RV structure and cell morphology or cell contractility (p > 0,05). However, the associated treatments reduced the amplitude of the [Ca2+]i transient (p < 0.05). In conclusion, the association of aerobic exercise training with MSCs therapy did not affect the right ventricular morphology and function of rats with myocardial infarction induced in the left ventricle.