Heart mitochondrial function in thyroid desoredr and hypovolemia

OGNOWSKI N; PUCHULU MB; BALASZCZUK AM; ZAOBORNYJ T; ZOTTA E; RUKAVINA MIKUSIK IA; VALDEZ LB; FELLET A

Congreso; Reunion Conjunta de Sociedades de Biociencias; 2017

Cardiovascular system regulation would be crucial in pathological situations such as hypovolemia. The actions of thyroid hormones would be relevant during this condition considering its actions on cellular respiration and mitochondrial function. The aim of the present work was to examine the effect of thyroid state on rat heart mitochondria function during hypovolemia. Sprague-Dawley rats aged 2 months old treated with T3 (hyper, 20 μg/100 g body weight) or 0.02% methimazole (hypo, w/v) during 28 days. Hypovolemic state was induced by a loss of 20% of blood volume during 2 minutes. Hearts were removed for mitochondria isolation and determination of O2 uptake, enzyme activity of complex I and protein levels (mtNOS, akt T and akt P). The malate-glutamate-supported state 3 respiration decreased and increased in hypo and Hyper rats. Hemorrhage did not change this parameter. Malate-glutamate-supported state 4 did not change. No differences in succinate-supported state 4 and 3 respiration were observed in all groups. Hypothyroidism increased nNOS protein levels. This protein levels did not change in Hyper animals. Withdrawal decreased and increased nNOS protein levels in hypo and Hyper rats, respectively. Hyper increased complex I activity and hemorrhage did not change this activity. No differences were observed between Eut and hypo rats. Hemorrhage only increased complex I activity in hypo group. Thyroid disorders increased aktT protein levels. Hemorrhage did not change this parameter. Hyper increased akt P protein levels meanwhile hemorrhage induced a decreased of this protein levels. In hypothyroidism the lowest NO production would be responsible for increasing cellular respiration and guaranteeing the supply of oxygen to the tissues. The opposite would happen in the hyperthyroid where high levels of NO try to decrease the oxygen consumption as in the euthyroid. Alterations of complex I activity as well as AKT pathway could mediate these effects.