Functional Effects of Hyperthyroidism on Cardiac Papillary Muscle in Rats

• Main Authors: Fabricio Furtado Vieira, Robson Ruiz Olivoto, Priscyla Oliveira da Silva, Julio Cesar Francisco, Rosalvo Tadeu Hochmuller Fogaça
• Format: Article
• Language: English
• Published: Sociedade Brasileira de Cardiologia (SBC)
• Series: Arquivos Brasileiros de Cardiologia
• Subjects: Hipertireoidismo / metabolismo; Ratos; Miocárdio; Contração Miocárdica; Hormônios Tireóideos
• Online Access: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2016004500542&lng=en&tlng=en

Abstract Background: Hyperthyroidism is currently recognized to affect the cardiovascular system, leading to a series of molecular and functional changes. However, little is known about the functional influence of hyperthyroidism in the regulation of cytoplasmic calcium and on the sodium/calcium exchanger (NCX) in the cardiac muscle. Objectives: To evaluate the functional changes in papillary muscles isolated from animals with induced hyperthyroidism. Methods: We divided 36 Wistar rats into a group of controls and another of animals with hyperthyroidism induced by intraperitoneal T3 injection. We measured in the animals' papillary muscles the maximum contraction force, speed of contraction (+df/dt) and relaxation (-df/dt), contraction and relaxation time, contraction force at different concentrations of extracellular sodium, post-rest potentiation (PRP), and contraction force induced by caffeine. Results: In hyperthyroid animals, we observed decreased PRP at all rest times (p < 0.05), increased +df/dt and -df/dt (p < 0.001), low positive inotropic response to decreased concentration of extracellular sodium (p < 0.001), reduction of the maximum force in caffeine-induced contraction (p < 0.003), and decreased total contraction time (p < 0.001). The maximal contraction force did not differ significantly between groups (p = 0.973). Conclusion: We hypothesize that the changes observed are likely due to a decrease in calcium content in the sarcoplasmic reticulum, caused by calcium leakage, decreased expression of NCX, and increased expression of a-MHC and SERCA2.