We examined the reversibility of these changes after the establishment

The 6-propyl-2-thiouracil drug which is a thiouracilderivative used to treat hyperthyroidism has been long used to induce hypothyroidism in animal models such as the rat. Data obtained from animal models on the Norethindrone effect of thyroid hormone on myocardial gene expression are further supported by clinical studies on humans. Most studies on the cardiovascular effects of thyroid hormones have particularly targeted left ventricular improvement. Nonetheless, little is known about the effect of an excess or deficiency of thyroid hormones on the myocardium collagen gene and the responsiveness of interstitial cells to these hormones. One study, however, showed that long term hypothyroidism caused overall cardiac muscle stiffness and left ventricle diastolic wall thickness due to increased collagen I/III-based stiffness. Furthermore, to our knowledge, no studies have evaluated the combined effect of hypothyroidism and thyroid hormone therapy on cardiac inflammation. The purpose of this study was to evaluate the cardiac fibrosis, inflammation and dysfunction caused by PTUinduced hypothyroidism in adult rats. Additionally, we examined the reversibility of these changes after the establishment of a euthyroid state. Gross examination and histological sections were analyzed by two independent pathologists in a blinded fashion. A Butenafine hydrochloride semiquantitative scoring system was used to assess the cardiac myocyte hypertrophy, tissue inflammation and fibrosis. Inflammation refers to the presence of aggregates of leukocytes in the heart muscle. Fibrosis analysis was performed by applying a threshold to the acquired pictures and creating selections of the fibrotic areas. Eight sections were analyzed for each rat in the three groups. Our study showed that hypothyroidism in rats is related to the development of cardiac fibrosis and inflammation along with chamber dilation and function decline. Interestingly, the rapid reestablishment of euthyroidism resulted in aggravated cardiac inflammation and injury, although the fibrosis and function were contradictorily ameliorated.