{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:20:50Z","timestamp":1787016050430,"version":"build-2736575974"},"reference-count":79,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2021,10,21]],"date-time":"2021-10-21T00:00:00Z","timestamp":1634774400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2021,11]]},"abstract":"<jats:sec>\n                    <jats:title>New Findings<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            <jats:bold>What is the central question of this study?<\/jats:bold>\n                          <\/jats:p>\n                          <jats:p>3,5\u2010Diiodothyronine (3,5\u2010T2) 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?<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            <jats:bold>What is the main finding and its importance?<\/jats:bold>\n                          <\/jats:p>\n                          <jats:p>Chronic 3,5\u2010T2 administration has no adverse effects on cardiac function. Remarkably, 3,5\u2010T2 improves the autonomous control of the rat heart and protects against ischaemia\u2013reperfusion injury.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>The use of 3,5,3\u2032\u2010triiodothyronine (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\u2010diiodothyronine (3,5\u2010T2) administration increases resting metabolic rate, prevents or treats liver steatosis in rodent models and ameliorates insulin resistance, suggesting 3,5\u2010T2 as a potential therapeutic tool. However, a comprehensive assessment of cardiac electrical and contractile properties has not been made so far. Three\u2010month\u2010old Wistar rats were daily administered vehicle, 3,5\u2010T2 or 3,5\u2010T2+T4 and no signs of atrial or ventricular arrhythmia were detected in non\u2010anaesthetized rats during 90\u00a0days. Cardiac function was preserved as heart rate, left ventricle diameter and shortening fraction in 3,5\u2010T2\u2010treated rats compared to vehicle and 3,5\u2010T2+T4 groups. Power spectral analysis indicated an amelioration of the heart rate variability only in 3,5\u2010T2\u2010treated rats. An increased baroreflex sensitivity at rest was observed in both 3,5\u2010T2\u2010treated groups. Finally, 3,5\u2010T2 Langendorff\u2010perfused hearts presented a significant recovery of left ventricular function and remarkably smaller infarction area after ischaemia\u2013reperfusion injury. In conclusion, chronic 3,5\u2010T2 administration ameliorates tonic cardiac autonomic control and confers cardioprotection against ischaemia\u2013reperfusion injury in healthy male rats.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/ep089589","type":"journal-article","created":{"date-parts":[[2021,10,4]],"date-time":"2021-10-04T19:10:49Z","timestamp":1633374649000},"page":"2185-2197","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["3,5\u2010Diiodothyronine protects against cardiac ischaemia\u2013reperfusion injury in male rats"],"prefix":"10.1113","volume":"106","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1789-4234","authenticated-orcid":false,"given":"Ruy Andrade","family":"Louzada","sequence":"first","affiliation":[{"name":"Laborat\u00f3rio de Fisiologia End\u00f3crina Doris Rosenthal Instituto de Biof\u00edsica Carlos Chagas Filho Universidade Federal do Rio de Janeiro  Rio de Janeiro 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