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Direct action of T₃ on phosphorylation potential in the sheep heart in vivo

¹Division of Cardiology, Department of Pediatrics, University of Washington School of Medicine, and ²Children's Hospital and Regional Medical Center, Seattle, Washington

Submitted 19 August 2004 ; accepted in final form 20 December 2004

Thyroid acting through ligand binding to nuclear receptors modifies myocardial respiratory kinetics and oxidative phosphorylation in the heart. Direct nongenomic action of thyroid hormone on high-energy phosphate concentrations and respiratory kinetics has never been proven in vivo but might be responsible for observed changes in oxygen utilization efficiency immediately after triiodothyronine (T₃) administration. We tested the hypothesis that T₃ directly and rapidly modifies myocardial high-energy phosphate concentrations and phosphorylation potential in vivo. Anesthetized sheep (age 28–40 days) thyroidectomized shortly after birth (Thy) and euthyroid age-matched controls (Con) underwent median sternotomy and received T₃ infusion (0.8 µg/kg), followed by epinephrine infusion to increase myocardial oxygen consumption (MO₂). ³¹P magnetic resonance spectra were monitored via a surface coil over the left ventricle. T₃ increased phosphocreatine (PCr)/ATP and decreased ADP in Thy animals without causing a change in MO₂. T₃ produced no changes in high-energy phosphates in Con animals. T₃ did not modify the PCr/ATP or ADP response to epinephrine and elevation in MO₂ in either group. Cardiac mitochondria isolated from Thy and Con animals showed no change in respiratory rate or ADP/ATP exchange efficiency after T₃ incubation. T₃ infusion in a hypothyroid state decreases ADP concentration, thereby altering the equilibrium between phosphorylation potential and myocardial respiratory rate. These T₃-induced effects are not due to changes in ADP/ATP exchange efficiency through action at the adenine nucleotide translocator but may be due to T₃ mediation of substrate utilization, confirmed in other models.

adenine nucleotide translocator; myocardial energy metabolism; substrate oxidation

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