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 6weeks, or co-treated with the vasodilator dipyridamole and PTU for 6weeks, or treated with PTU for 6weeks and treatment discontinued for 2 or 4weeks. 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 3weeks treatment and 34% by 6weeks which was largely reversed after discontinuing PTU treatment for only 2weeks. 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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