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3,5-Diiodothyronine protects against cardiac ischaemia-reperfusion injury in male rats.

AbstractNEW FINDINGS:
What is the central question of this study? 3,5-Diiodothyronine (3,5-T2) administration increases resting metabolic rate, prevents or treats liver steatosis in rodent models, and ameliorates insulin resistance: what are its effects on cardiac electrical and contractile properties and autonomic regulation? What is the main finding and its importance? Chronic 3,5-T2 administration has no adverse effects on cardiac function. Remarkably, 3,5-T2 improves the autonomous control of the rat heart and protects against ischaemia-reperfusion injury.
ABSTRACT:
The use of 3,5,3'-triiodothyronine (T3) and thyroxine (T4) to treat metabolic diseases has been hindered by potential adverse effects on liver, lipid metabolism and cardiac electrical properties. It is recognized that 3,5-diiodothyronine (3,5-T2) administration increases resting metabolic rate, prevents or treats liver steatosis in rodent models and ameliorates insulin resistance, suggesting 3,5-T2 as a potential therapeutic tool. However, a comprehensive assessment of cardiac electrical and contractile properties has not been made so far. Three-month-old Wistar rats were daily administered vehicle, 3,5-T2 or 3,5-T2+T4 and no signs of atrial or ventricular arrhythmia were detected in non-anaesthetized rats during 90 days. Cardiac function was preserved as heart rate, left ventricle diameter and shortening fraction in 3,5-T2-treated rats compared to vehicle and 3,5-T2+T4 groups. Power spectral analysis indicated an amelioration of the heart rate variability only in 3,5-T2-treated rats. An increased baroreflex sensitivity at rest was observed in both 3,5-T2-treated groups. Finally, 3,5-T2 Langendorff-perfused hearts presented a significant recovery of left ventricular function and remarkably smaller infarction area after ischaemia-reperfusion injury. In conclusion, chronic 3,5-T2 administration ameliorates tonic cardiac autonomic control and confers cardioprotection against ischaemia-reperfusion injury in healthy male rats.
AuthorsRuy Andrade Louzada, Alvaro Souto Padron, Silvio Rodrigues Marques-Neto, Leonardo Maciel, João Pedro Werneck-de-Castro, Andrea Claudia Freitas Ferreira, Jose Hamilton Matheus Nascimento, Denise Pires Carvalho
JournalExperimental physiology (Exp Physiol) Vol. 106 Issue 11 Pg. 2185-2197 (11 2021) ISSN: 1469-445X [Electronic] England
PMID34605090 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2021 The Authors. Experimental Physiology © 2021 The Physiological Society.
Chemical References
  • Diiodothyronines
  • 3,5-diiodothyronine
Topics
  • Animals
  • Diiodothyronines (pharmacology, therapeutic use)
  • Heart
  • Male
  • Myocardial Reperfusion Injury (metabolism)
  • Rats
  • Rats, Wistar

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