Função ventricular direita de corações isolados de ratos com e sem sinais de insuficiência cardíaca oito semanas após infarto agudo do miocárdio

• Ano de defesa: 2007
• Autor(a) principal: Moura, Viviane Guimarães Carvalho de
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal do Espírito Santo; BR; Mestrado em Ciências Fisiológicas; Centro de Ciências da Saúde; UFES; Programa de Pós-Graduação em Ciências Fisiológicas
• Palavras-chave em Português: Insuficiência cardíaca; Coração isolado; Ratos; Coração - Ventrículos; Infarto do miocárdio; Rato como animal de laboratório; Fisiologia; 612
• Link de acesso: http://repositorio.ufes.br/handle/10/7926

Recent studies performed in our laboratory the demonstrated that rats submitted to myocardial infarction (MI), presenting same infarct area, may develop or not heart failure (HF). Moreover, the study of right ventricle (RV) isolated strips showed that contractility is preserved following MI in rats without HF signals with similar infarct area. However, it is unknown if such response occurs in the isolated heart preparation. In Langendorff perfused hearts is possible to evaluate the contractile performance by using inotropic interventions independent of any extrinsic mechanism of contractility control. Thus, the aim of the present study was to investigate the RV performance of hearts under isovolumetric contraction of rats with and without HF signs after 8 weeks of MI. Male Wistar rats were divided in three groups: control (SHAM, n= 11); infarction without HF signs (INF, n= 11) and infarction with HF signs (HF, n= 11). The in vivo results showed improvement of RV function in the HF group (RVSP= 48 ± 2.2* mmHg; RVEDP= 4.5 ± 0.8*; mmHg; dP/dt+= 2046 ± 226* mmHg/s; dP/dt- =1807 ± 84* mmHg/s; *p<0.05). In the INF group the RV function remained unaltered (RVSP= 31 ± 2.6 mmHg; VEDP= 1.2 ± 0.4 mmHg; dP/dt+= 1192 ± 165 mmHg/s; dP/dt-= 1239 ± 156 mmHg/s). The HF group included the animals that presented increase in LVEDP (HF= 13.0 ± 1.8* vs. INF=2.6 ± 0.5; SHAM= 3.2 ± 0.4 mmHg; *p<0.05), RV hypertrophy and increase on wet weight of lungs. The infarct area was similar between groups (INF= 27.6 ± 1.2 e HF= 29.2 ± 0.8%). Nevertheless, in vitro results were different of those obtained in vivo. The heterometric mechanism of contractility regulation, obtained by stretch-tension curve (DP= 0 - 30 mmHg, and the homeometric mechanism, obtained by [Ca+2]e response concentration curve (0.62 mM – 3.75 mM) and isoproterenol administration (5x10-5 M), were impaired in the RV HF animals. The main results presented here demonstrated that infarcted rats with HF signs presented better RV performance in vivo than in vitro. These findings suggest that, in the HF animals, the neurohumoral mechanisms are important to maintain the heart function. Second, INF rats presenting the same infarct area, showed a normal RV function in vivo, wich suggest that, in these animals, the HF are not dependent on the infarct size.