Triiodothyronine (T3) improves ischemic-reperfused myocardium recovery by enhancing AMP-activated protein kinase (AMPK) activation

HERMANN, ROMINA; CORDOBA, MAILEN FLORENCIA; MARINA PRENDES, MARIA GABRIELA; REZNIK, FEDERICO JOAQUIN; VELEZ, DEBORA; FERNANDEZ PAZOS, MARIA DE LAS MERCEDES; MESTRE CORDERO, VICTORIA

La Habana

Congreso; 2nd Pan-American Congress of Physiological Sciences; 2019

American Physiological Society

Low T3 syndrome is the most frequent alterationof thyroid hormone metabolism in acute myocardial infarction, which occursimmediately after the onset of symptoms. Although low T3 state has beeninterpreted as a merely adaptive mechanism, the experimental and clinical datahave rebutted this hypothesis, suggesting that T3 might play an effective rolein the cardioprotection against ischemia-reperfusion injury. Recent studieshave provided evidence that T3 could enhance the recovery of ischemicmyocardium through the preservation of mitochondrial function and theimprovement of energy substrate metabolism. To this respect, it has beensuggested that T3 could activate AMPK, the cellular ?fuel gauge? enzyme, whichin previous studies carried out in our laboratory exerted protective effectsfor the recovery of ischemic-reperfused myocardium. The aim of the present study was to investigatethe effects produced by the acute treatment with T3 and the pharmacologicalinhibition of AMPK by Compound C (CC), on isolated rat left atria subjected tosimulated ischemia-reperfusion.For this aim the atria were incubated inKrebs?Ringer containing 10 mM glucose, 95% O2?5% CO2, pH7,4. For Is, the incubation medium contained 10 mM 2-deoxy-D-glucose, 95% N2?5%CO2, pH 6,8. ANOVA, followed by Tukey?s test, was used, n=8/group.Results showed that T3 increased AMPK activationduring Is, which was prevented by CC (End stabilization period (ESP): 1.50 ± 0.09,Is-Rs: 2.34 ± 0.02*, Is-Rs+T3: 2.70 ± 0.07*#, Is-Rs+CC: 1.30 ± 0.08,Is-Rs+T3+CC: 1.33 ± 0.07 AU; *p