Ischemic cardiomyopathy and thyroid alterations: from the energetics of calcium homeostasis to cardioprotection in rat cardiac models.

RAGONE MI.; COLAREDA GE; BAYLEY M; BONAZZOLA P; LOPEZ S; CONSOLINI A.E.

Mar del Plata

Congreso; Reunión de Biociencias 2019; 2019

SAFE

Thyroid diseases affect cardiac Ca2+ homeostasis and induce long-term pathologies such as hypertrophy and remodelation. The consequences of cardiac ischemia-reperfusion (I/R) are still worse in a hyper- or a hypothyroid patient. The aim of this project is to characterize the myocardial mechanisms of hyperthyroidism (HypT) and hypothyroidism (HypoT) in the postischemic dysfunction, especially the mitochondrial role in two models of stunning due to I/R. HypT rats were obtained by daily SC injection of 20 μg.kg-1 triyodothyronine, and HypoT rats by drinking 0.02% methymazol, both during 15 days. Results were compared with rats without treatment (euthyroid, EuT). Ventricles were perfused in a flow calorimeter (37ºC-3Hz). Intraventricular contractile pressure (P, mmHg), diastolic contracture (ΔLVEDP) and total heat rate (Ht, mW.g-1) were measured, and the total muscle economy (Eco=P/Ht) was calculated. Isolated hearts were exposed to one of two models of I/R: moderate (20 min I) or severe (30 min I) followed by 45 min R (mI/R or sI/R, respectively). HypT was cardioprotector in mI/R because it increased the post-ischemic contractile recovery (PICR) to 108±12% of preischemic P (vs 70±6% in EuT, p