Key result
Thyroid disorders were associated with hypertrophic remodelling impacting cardiac function, while hypovolemia triggered nitric oxide synthase activation to maintain haemodynamic homeostasis.
Why the study?
Does nitric oxide participate in the cardiovascular function and haemodynamic adaptation to acute haemorrhage in animals with thyroid disorders?
Does nitric oxide participate in the cardiovascular function and haemodynamic adaptation to acute haemorrhage in animals with thyroid disorders?
In a rat model, thyroid disorders alter cardiac remodeling and adaptation to hypovolemia, with nitric oxide synthase activation playing a key role in maintaining hemodynamic homeostasis.
Answers are grounded in this paper and cite their sources.
Thyroid-cardiac interactions in rats highlight nitric oxide's potential compensatory role; leaves open translation to human hypovolemia management.
This study aimed to investigate whether nitric oxide participates in the cardiovascular function and haemodynamic adaptation to acute haemorrhage in animals with thyroid disorders. Sprague-Dawley rats aged 2months old treated with T3 (hyper, 20μg/100g body weight) or 0.02% methimazole (hypo, w/v) during 28days were pre-treated with N(G) 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. Haemorrhage elicited a hypotension of similar magnitude within 10min. Then, this parameter was stabilized at about 30-40min and maintained until finalized, 120min. 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 isoform in hypo. In ventricle, hyper and hypo had a higher enzyme activity, which was not correlated with changes in protein levels. Haemorrhage induced an increased heart nitric oxide production. We concluded that thyroid disorders were associated with hypertrophic remodelling which 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.
No takes yet. Share an insight, caveat, or question.
Ogonowski et al. (2016) studied Thyroid disorders and acute haemorrhage. T3 or methimazole followed by L-NAME and 20% blood loss was evaluated on Cardiovascular function and haemodynamic adaptation to acute haemorrhage. Thyroid disorders were associated with hypertrophic remodelling impacting cardiac function, while hypovolemia triggered nitric oxide synthase activation to maintain haemodynamic homeostasis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: