Cardioprotective doses of thyroid hormones improve NO bioavailability in erythrocytes and increase HIF-1α expression in the heart of infarcted rats.
Alexandre Luz de CastroRafael Oliveira FernandesVanessa D OrtizCristina Campos-CarraroJéssica H P BonettoTânia Regina G FernandesAdriana ConzattiRafaela SiqueiraAngela Vicente TavaresAdriane Bello KleinAlex Sander da Rosa AraujoPublished in: Archives of physiology and biochemistry (2020)
Context: Infarction leads to a decrease in NO bioavailability in the erythrocytes. Thyroid hormones (TH) present positive effects after infarction. However, there are no studies evaluating the effects of cardioprotective doses of TH in the erythrocytes after infarction.Objective: This study aimed to evaluate the effects of TH in NO bioavailability and oxidative stress parameters in the erythrocytes of infarcted rats.Material and methods: Wistar rats were allocated into the three groups: Sham-operated (SHAM), infarcted (AMI) and infarcted + TH (AMIT). AMIT rats received T4 and T3 for 12 days by gavage. Subsequently, the animals were evaluated by echocardiography and the LV and erythrocytes were collected.Results: TH improved NO bioavailability and increased catalase activity in the erythrocytes. Besides that, TH increased HIF-1α in the heart.Conclusion: TH seems to be positive for erythrocytes preventing a decrease in NO bioavailability and increasing antioxidant enzymatic defense after infarction.