Cardiac ischemia/reperfusion injury is inversely affected by thyroid hormones excess or deficiency in male Wistar rats

• Published in: PloS one Vol. 13; no. 1; p. e0190355
• Main Authors: Seara, Fernando A C, Maciel, Leonardo, Barbosa, Raiana A Q, Rodrigues, Nayana C, Silveira, Anderson L B, Marassi, Michelle P, Carvalho, Adriana B, Nascimento, José Hamilton M, Olivares, Emerson L
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01-01-2018; Public Library of Science (PLoS)
• Subjects: Animals; Antioxidants; Biology; Biology and Life Sciences; Biophysics; Blood pressure; Cardiology; Cardiovascular disease; Catalase; Coronary vessels; Diastolic pressure; Drinking water; Enzymes; Glutathione; Glutathione peroxidase; Heart; Hormones; Hypertrophy; Hypothyroidism; Infarction; Injuries; Ischemia; Laboratory animals; Male; Mechanical properties; Medicine and Health Sciences; mRNA; Myocardial ischemia; Myocardial Reperfusion Injury - blood; Myocardial Reperfusion Injury - pathology; Peroxidase; Pharmacology; Physiology; Polymerase chain reaction; Rats; Rats, Wistar; Reperfusion; Reverse Transcriptase Polymerase Chain Reaction; Superoxide dismutase; Systolic pressure; Thyroid; Thyroid gland; Thyroid hormones; Thyrotoxicosis; Thyroxine; Thyroxine - blood; Triiodothyronine - blood; Ventricle; Workloads; Brazil; United States > US; Rio de Janeiro Brazil
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0190355

Thyroid dysfunctions can increase the risk of myocardial ischemia and infarction. However, the repercussions on cardiac ischemia/reperfusion (IR) injury remain unclear so far. We report here the effects of hypothyroidism and thyrotoxicosis in the susceptibility to IR injury in isolated rat hearts compared to euthyroid condition and the potential role of antioxidant enzymes.
Hypothyroidism and thyrotoxicosis were induced by administration of methimazole (MMZ, 300 mg/L) and thyroxine (T4, 12 mg/L), respectively in drinking water for 35 days. Isolated hearts were submitted to IR and evaluated for mechanical dysfunctions and infarct size. Superoxide dismutase types 1 and 2 (SOD1 and SOD2), glutathione peroxidase types 1 and 3 (GPX 1 and GPX3) and catalase mRNA levels were assessed by quantitative RT-PCR to investigate the potential role of antioxidant enzymes.
Thyrotoxicosis elicited cardiac hypertrophy and increased baseline mechanical performance, including increased left ventricle (LV) systolic pressure, LV developed pressure and derivatives of pressure (dP/dt), whereas in hypothyroid hearts exhibited decreased dP/dt. Post-ischemic recovery of LV end-diastolic pressure (LVEDP), LVDP and dP/dt was impaired in thyrotoxic rat hearts, whereas hypothyroid hearts exhibited improved LVEDP and decreased infarct size. Catalase expression was decreased by thyrotoxicosis.
Thyrotoxicosis was correlated, at least in part, to cardiac remodeling and increased susceptibility to IR injury possibly due to down-regulation of antioxidant enzymes, whereas hypothyroid hearts were less vulnerable to IR injury.