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

Autor: Adriana Bastos Carvalho, Leonardo Maciel, Raiana A. Q. Barbosa, José Nascimento, Anderson Luiz Bezerra da Silveira, Emerson L. Olivares, Nayana Coutinho Rodrigues, Fernando A.C. Seara, Michelle P. Marassi
Rok vydání: 2018
Předmět:
Male
0301 basic medicine
GPX3
lcsh:Medicine
Blood Pressure
030204 cardiovascular system & hematology
Vascular Medicine
Biochemistry
Antioxidants
Endocrinology
0302 clinical medicine
Ischemia
Medicine and Health Sciences
lcsh:Science
chemistry.chemical_classification
Multidisciplinary
Triiodothyronine
Reverse Transcriptase Polymerase Chain Reaction
Glutathione peroxidase
Heart
Systolic Pressure
Enzymes
Dismutases
Anatomy
Research Article
medicine.medical_specialty
Cardiac Ventricles
Endocrine Disorders
Myocardial Reperfusion Injury
03 medical and health sciences
Hypothyroidism
Internal medicine
medicine
Animals
Rats
Wistar

Euthyroid Condition
Superoxide Dismutase
business.industry
lcsh:R
Biology and Life Sciences
Proteins
medicine.disease
Rats
Thyroxine
Preload
030104 developmental biology
Blood pressure
chemistry
Cardiovascular Anatomy
Enzymology
lcsh:Q
business
Reperfusion injury
Catalases
Zdroj: PLoS ONE, Vol 13, Iss 1, p e0190355 (2018)
PLoS ONE
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0190355
Popis: Aim 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. Methods 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. Results 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. Conclusion 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.
Databáze: OpenAIRE