ACUTE TREATMENT WITH TRIIODOTHYRONINE (T3) ATTENUATES POSTISCHEMIC MITOCHONDRIAL INJURY: A RESPONSE ASSOCIATED WITH ENHANCED AMP-ACTIVATED PROTEIN KINASE (AMPK) ACTIVATION.

HERMANN R.; CÓRDOBA M.; FELLET A.; REZNIK F.; VÉLEZ D.; FERNÁNDEZ PAZOS MM.; MESTRE CORDERO V.; MARINA PRENDES MG.

Mar del Plata

Congreso; Reunion Conjunta SAIC SAFE SAB SAP 2019; 2019

SAIC SAFE SAB SAP

Recent studies have provided evidence that acute treatment with T3 could enhance the recovery of ischemic myocardium through the preservation of mitochondrial function and the improvement of energy substrate metabolism. To this respect, our previous results showed that T3 enhanced the activation of AMPK, a key enzyme that regulates the cellular energy metabolism, during Is-Rs, which was prevented by AMPK pharmacological inhibitor, Compound C (CC; 10 μM). During reperfusion, T3 increased contractile function recovery, mitochondrial ATP production and tissue ATP, effects that were reverted by CC.The aim of the present study was to investigate the effects produced by the acute treatment with T3 (60 nM) and AMPK inhibitor, in mitochondria of isolated rat left atria subjected to 75 min simulated ischemia (Is)?75 min reperfusion (Rs). ANOVA, followed by Tukey?s test was used, n=8/group.The results showed that mitochondrial ultrastructure, analyzed by electron microscopy, was better preserved in the atria subjected to Is-Rs in the presence T3, effect that was reverted by CC. Moreover, calcium retention capacity (CRC), defined as the amount of Ca2+ required to trigger a massive Ca2+ release by isolated mitochondria, was increased by acute treatment with T3, effect that was reverted by CC (Is-Rs:77±9, Is-Rs+T3:114±12*, Is-Rs+T3+CC:82±8 nmol/mg protein; *p