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Hyperthyroidism is accompanied by important changes in hemodynamics and cardiac functions. These include clinical manifestation such as an increased cardiac contractility and heart rate, as well as decreased peripheral vascular resistance. Increased nitric oxide production [1,2], which may affect the peripheral vascular resistance, and shorter time-to-peak of twitch tension, which may be associated with an increased cardiac contractility, have been reported in the hyperthyroid state [3]. Thyroid hormone is also known to affect the gene expression; major components of myocardial contraction, including sarcoplasmic reticulum (SR) Ca 2ϩ -ATPase (SERCA2) [4]; myosin heavy chains (MHC) [5]; and other protein expressions, such as glucose transporter GLUT4 facilitating glucose uptake [6]. Glucose metabolism is very important to providing energy not only for myocardial contraction, but also for the maintenance of intracellular ionic balances.Thyroid hormone is a potential contributor to a bet- Japanese Journal of Physiology, 53, 411-416, 2003 Key words: hyperthyroidism, myocardial metabolism, SR Ca 2ϩ ATPase, excitation-contraction coupling. Abstract:Hyperthyroidism is known to affect multiple organ functions, and thyroid hormone has been known to improve myocardial function in a failing heart. The purpose of this study is to elucidate the functional and metabolic effects of thyroid hormone on myocardium in a rat model exposed to long-term excess thyroid hormone, particularly focusing on the SR Ca 2ϩ -ATPase (SERCA2) function. 3,5,3Ј-Triiodo-L-thyronine (T3), or the vehicle, was subcutaneously given for 4 weeks (T3 and control [C] group). Bolus I.V. Thapsigargin (TG) was used to test the SERCA2 function (C-TG and T3-TG) in Langendorff perfused heart. Myocardial functions such as LVdeveloped pressure (LVDP; mmHg), ϮdP/dt (mmHg/s), (ms), and oxygen consumption (MVO 2 ; ml/min/g wt) were measured. SERCA2 and GLUT4 protein level were also evaluated by Western immunoblotting. Left ventricle to body weight (LV/BW) ratio was significantly higher in the T3 group. Both negative dP/dt and were significantly decreased by TG. It is interesting that the decrement of negative dP/dt and attained by TG was significantly larger in the hyperthyroid group (T3-TG) than in a normal heart (C-TG). SERCA2 and GLUT4 protein levels were not significantly different between control and the T3 group. We conclude that prolonged exposure to thyroid hormone causes hypertrophy of the myocardium and an augmentation of the SR Ca 2ϩ ATPase activity. Care must be taken in hyperthyroid heart during the ischemia-reperfusion process where the SRECA2 function is inhibited.

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