Key result
l-thyroxine-induced hyperthyroidism caused structural capillary rarefaction, down-regulation of cardiac angiotensin II AT1 receptor, LV dysfunction, and cardiac hypertrophy in rats.
Why the study?
Does l-thyroxine-induced hyperthyroidism cause cardiac microvascular rarefaction and LV dysfunction in male Wistar rats?
Does l-thyroxine-induced hyperthyroidism cause cardiac microvascular rarefaction and LV dysfunction in male Wistar rats?
Hyperthyroidism induces cardiac microvascular rarefaction and down-regulates angiotensin II AT1 receptors, which may contribute to hyperthyroidism-induced LV dysfunction.
Rat findings warrant no practice change; leaves open microvascular role in human hyperthyroid cardiomyopathy.
OBJECTIVE: The pathophysiology underlying hyperthyroidism-induced left ventricle (LV) dysfunction and hypertrophy directly involves the heart and indirectly involves the neuroendocrine systems. The effects of hyperthyroidism on the microcirculation are still controversial in experimental models. We investigated the effects of hyperthyroidism on the cardiac function and microcirculation of an experimental rat model. METHODS: Male Wistar rats (170-250 g) were divided into two groups: the euthyroid group (n = 10), which was treated with 0.9% saline solution, and the hyperthyroid group (n = 10), which was treated with l-thyroxine (600 μg/kg/day, i.p.) during 14 days. An echocardiographic study was performed to evaluate the alterations in cardiac function, structure and geometry. The structural capillary density and the expression of angiotensin II AT1 receptor in the LV were analyzed using histochemistry and immunohistochemistry, respectively. RESULTS: Hyperthyroidism was found to induce profound cardiovascular alterations, such as systolic hypertension, tachycardia, LV dysfunction, cardiac hypertrophy, and myocardial fibrosis. This study demonstrates the existence of structural capillary rarefaction and the down-regulation of the cardiac angiotensin II AT1 receptor in the myocardium of hyperthyroid rats in comparison with euthyroid rats. CONCLUSIONS: Microvascular rarefaction may be involved in the pathophysiology of hyperthyroidism-induced cardiovascular alterations.
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Freitas et al. (2013) studied Hyperthyroidism-induced left ventricle dysfunction (n=20). l-thyroxine vs. 0.9% saline solution was evaluated on Cardiac function, structure and geometry, structural capillary density, and expression of angiotensin II AT1 receptor. l-thyroxine-induced hyperthyroidism caused structural capillary rarefaction, down-regulation of cardiac angiotensin II AT1 receptor, LV dysfunction, and cardiac hypertrophy in rats.
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