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

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

Mendoza

Simposio; II Simposio Internacional de Medicina Traslacional; 2019

Facultades de Ciencias Médicas y de Ciencias Exactas y Naturales de la UNCuyo, Facultad de Farmacia y Bioquímica de la UBA, Facultad de Medicina de la Albert-Ludwigs-Universität de Freiburg (Alemania) y la Secretaría de Investigación, Internacionales y Po

Recent studies have provided evidence that T3 enhances the recovery of ischemic myocardium through the preservation of mitochondrial function and the improvement of energy substrate metabolism. To this respect, it has been suggested that T3 might activate AMPK, the cellular ?fuel gauge? enzyme, which in previous studies carried out in our laboratory exerted protective effects for the recovery of ischemic-reperfused myocardium. The aim of the present study was to investigate the effects produced by the acute treatment with T3 and the pharmacological inhibition of AMPK by Compound C (CC), on isolated rat left atria subjected to 75 min simulated ischemia-75 min reperfusion (Is-Rs).Atria were incubated in Krebs?Ringer containing 10 mM glucose, 95% O2?5% CO2, pH 7.4. For Is, the incubation medium contained 10 mM 2-deoxy-D-glucose, 95% N2?5% CO2, pH 6.8. T3 (60 nM) and CC (10 M) were added to the bathing medium at the onset of Is and maintained throughout the experiment. ANOVA, followed by Tukey?s test, n=8/group.Results showed that T3 increased AMPK activation during Is, which was prevented by CC (End stabilization period (ESP):1.33±0.02, Is-Rs:2.20±0.11*, Is-Rs+T3:2.79±0.10*#, Is-Rs+CC:1.08±0.19, Is-Rs+T3+CC:1.17±0.10 AU;*p