Cardioprotective effects of thyroid hormones in a rat model of myocardial infarction are associated with oxidative stress reduction

• This study evaluated thyroid hormones effects in oxidative stress after infarction.
• T3 and T4 administration reduced ROS levels induced by myocardial infarction.
• This treatment also normalized cardiac redox status and prevented lipid peroxidation.
• This was associated with improved cardiac remodeling after the ischemic injury.
• Thus oxidative stress may have a relevant part in T3 and T4 cardioprotective effects.

Reactive oxygen species (ROS) are involved with progression from infarction to heart failure. Studies show that thyroid hormones (TH) present cardioprotective effects. This study aims to evaluate whether TH effects after infarction are associated to redox balance modulation. Male Wistar rats were divided into four groups: Sham-operated (SHAM), infarcted (AMI), sham-operated + TH (SHAMT), and infarcted + TH (AMIT). During 26 days, animals received T3 (2 μg/100 g/day) and T4 (8 μg/100 g/day) by gavage. Echocardiographic parameters were assessed and heart tissue was collected to biochemical analysis. AMIT rats presented absence of lung congestion, less cardiac dilatation, and normalization in myocardial performance index, compared with AMI. AMI rats presented an increase in hydrogen peroxide levels and in lipid peroxidation and a decrease in GSH/GSSG. TH prevented these alterations in AMIT. In conclusion, TH seem to reduce the levels of ROS, preventing oxidative stress, and improving cardiac function in infarcted rats.