CONICET | Buscador de Institutos y Recursos Humanos

The aim of this study was to investigate whether nitric oxide participate in the cardiovascular function and haemodynamic adaptation to acute hemorrhage in animals with thyroid disorders. Sprague-Dawley rats aged 2 months old treated with T3 (Hyper, 20ug/100g body weight) or 0.02% methimazole (hypo, w/v) during 28 days were pretreated with NG nitro-L-arginine methyl ester (L-NAME) and submitted to 20% blood loss. Heart function was evaluated by echocardiography. Measurements of arterial blood pressure, heart rate, nitric oxide synthase activity and protein levels were performed. We found that hypo decreased fractional shortening and ejection fraction and increased left ventricle internal diameter. Hyper decreased ventricle diameter and no changes in cardiac contractility. Hemorrhage elicited a hypotension of similar magnitude within the 10 min. Then, this parameter was stabilized at about 30-40 min and maintained until finalized 120 min. L-NAME rats showed that the immediate hypotension would be independent of nitric oxide. Nitric oxide synthase inhibition blunted the changes of heart rate induced by blood loss. Hyper and hypo had lower atrial enzyme activity associated with a decreased enzyme isoforms in hypo. In ventricle, Hyper and hypo had a higher enzyme activity which was not correlated with changes in protein levels. Hemorrhage induced an increase heart nitric oxide production. We conclude that thyroid disorders were associated with hypertrophic remodelling which was and impacted differently on cardiac function and its adaptation to a hypovolemia. Hypovolemia triggered a nitric oxide synthase activation modulating the heart function to maintain haemodynamic homeostasis. This involvement depends on a specific enzyme isoform, cardiac chamber and thyroid state.