Laboratório de Fisiologia Cardiovascular, Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Arch Physiol Biochem. 2022 Dec;128(6):1516-1523. doi: 10.1080/13813455.2020.1779752. Epub 2020 Jun 17.
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.
This study aimed to evaluate the effects of TH in NO bioavailability and oxidative stress parameters in the erythrocytes of infarcted rats.
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.
TH improved NO bioavailability and increased catalase activity in the erythrocytes. Besides that, TH increased HIF-1α in the heart.
TH seems to be positive for erythrocytes preventing a decrease in NO bioavailability and increasing antioxidant enzymatic defense after infarction.
梗死导致红细胞中 NO 生物利用度降低。甲状腺激素(TH)在梗死后具有积极作用。然而,目前尚无研究评估梗死后给予心脏保护剂量的 TH 对红细胞的影响。
本研究旨在评估 TH 对梗死大鼠红细胞中 NO 生物利用度和氧化应激参数的影响。
Wistar 大鼠分为三组:假手术组(SHAM)、梗死组(AMI)和梗死+TH 组(AMIT)。AMIT 大鼠通过灌胃给予 T4 和 T3 12 天。随后,通过超声心动图评估动物,并收集 LV 和红细胞。
TH 改善了红细胞中 NO 生物利用度,并增加了过氧化氢酶活性。此外,TH 增加了心脏中的 HIF-1α。
TH 似乎对红细胞有益,可防止梗死后 NO 生物利用度降低,并增加抗氧化酶防御。