Abstract

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.

中文翻译：

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心脏保护剂量的甲状腺激素可提高红细胞中 NO 的生物利用度并增加梗塞大鼠心脏中 HIF-1α 的表达

摘要

语境

梗塞导致红细胞中 NO 的生物利用度降低。甲状腺激素 (TH) 在梗塞后表现出积极作用。然而，没有研究评估心肌梗死后红细胞中 TH 的心脏保护剂量的影响。

客观的

本研究旨在评估 TH 对梗塞大鼠红细胞中 NO 生物利用度和氧化应激参数的影响。

材料与方法

将 Wistar 大鼠分为三组：假手术组 (SHAM)、梗死组 (AMI) 和梗死 + TH (AMIT)。AMIT 大鼠通过管饲法接受 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。

结果

TH 改善了 NO 的生物利用度并增加了红细胞中的过氧化氢酶活性。除此之外，TH 增加心脏中的 HIF-1α。

结论

TH 似乎对红细胞呈阳性，可防止 NO 生物利用度降低并增加梗塞后的抗氧化酶防御。