Abstract
Low thyroid function induced by either propylthiouracil (PTU) treatment or thyroidectomy surgery led to a reduction of arteriolar density in adult rat myocardium, which can be prevented by treatment with thyroxine or the thyroid hormone analogue 3,5-diiodothyropropionic acid (DITPA). However, many questions related to pathophysiological changes and the regulation of arteriolar density in the heart due to hypothyroidism remain unanswered. Sprague–Dawley rats were treated with PTU in drinking water for 1, 3, and 6 weeks, or co-treated with the vasodilator dipyridamole and PTU for 6 weeks, or treated with PTU for 6 weeks and treatment discontinued for 2 or 4 weeks. Heart mass, body mass, cardiac function and myocardial arteriolar density were determined. Arteriolar loss in hypothyroidism induced by PTU treatment progressed gradually with a 22% reduction after 3 weeks treatment and 34% by 6 weeks which was largely reversed after discontinuing PTU treatment for only 2 weeks. Combined treatment with the vasodilator dipyridamole during the 6-week PTU treatment period prevented vessel loss indicating the mechanism of arteriolar loss from hypothyroidism may result from vasoconstriction. These results suggest that thyroid hormone is a powerful regulator of vasculature in adult myocardium, particularly in low thyroid states.
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