Thyroid hormones and heart mitochondrial nitric oxide under hypovolemia

Abstract

After 28 days of treatment, the animals were anesthetized with urethane (1 g/kg ip). A tracheotomy was performed using polyethylene AbstractThe aim of the present work was to examine the effect of thyroid state on rat heart mitochondria function during hypovolemia. Sprague-Dawley rats treated with T 3 (hyper, 20 μg/100 g body weight) or 0.02% methimazole (hypo, w/v) for 28 days. Hypovolemia was induced by acute hemorrhage. O2 uptake, complex I activity and mitochondrial nitric oxide synthase (mtNOS) protein levels were determined in heart mitochondria. The malate-glutamate-supported state 3 respiration decreased and increased in hypo and hyperthyroid rats, while state 4 respirations did not change. Complex I activity and mtNOS protein levels were decreased in hypothyroid rats even in acute hypovolemia. Hyperthyroidism did not change these parameters. In summary, this study showed, for the first time, interesting findings that heart mitochondrial function is altered during thyroid disorder and acute hypovolemia. Heart mitochondrial nitric oxide, modulating oxygen uptake, may be involved in the adaptative response to assure the cardiomyocytes survives in this experimental condition. Citation: Ogonowski N, Valdez LB, Zaobornyj T, et al. Thyroid hormones and heart mitochondrial nitric oxide under hypovolemia.

Thyroid hormone disorder and the heart: The role of cardiolipin in calcium handling

“…We demonstrated that decreased TH level would probably be a hormonal environment that promotes changes in mitochondrial NO bioavailability modulating oxygen consumption and cell respiration. Alterations of complex I activity could mediate these effects (Ogonowski et al, 2018). We suggest that these mitochondrial alterations associated with thyroid disorder may be responsible for On the other hand, besides their function in energy conversion, mitochondria participate in multiple metabolic pathways, such as the urea cycle, the metabolism of amino acids and lipids, and the biogenesis of haem and iron sulfur clusters (Smith et al, 2018).…”

“…We demonstrated that decreased TH level would probably be a hormonal environment that promotes changes in mitochondrial NO bioavailability modulating oxygen consumption and cell respiration. Alterations of complex I activity could mediate these effects (Ogonowski et al., 2018 ). We suggest that these mitochondrial alterations associated with thyroid disorder may be responsible for cardiovascular alterations.…”