Thyroid Hormone in Neural Rescue

Abstract

Serum thyroxine (T₄), triiodothyronine (T₃), and reverse triiodothyronine (rT₃) were followed for 24 h in dogs resuscitated following 9 min of controlled cardiac arrest (CA). Total T₄, free T₄, total T₃, and free T₃ decreased, while reverse T₃ was elevated in the 24 h following resuscitation. Similar changes occurred with only 30 sec of CA. Levothyroxine sodium (L-T4) post-CA (7.5 μg/kg/h = CA + 7.5 or 15 μg/kg/h = CA + 15) increased total T₄, free T₄, and total T₃. Free T₃ decreased in the CA + 7.5 group but did not fall in CA + 15 group. Neurologic function improved significantly by 6 through 24 h (p < 0.05). Follow-up studies infusing T₃ or rT₃ failed to improve neurologic outcome. Systemic oxygen consumption (Vo₂) and delivery was assessed in a separate group of seven dogs that received a pre-CA L-T₄ infusion of 15 μ ug/kg/h for 1.5 h and L-T₄ infusion for 6 h afterward while controls (n = 7) received saline. Systemic Vo₂, VCO₂, and RQ were calculated from blood contents and cardiac output and serum levels of circulating TSH, T₄, FT₄, T₃, FT₃, and rT₃ were measured before L-T₄ and periodically over 6 h. L-T₄ maintained significantly higher T₄, FT₄, T₃, FT₃, rT₃, Vo₂, and cardiac output compared to controls. No change in canine TSH was detected. Rapid and dramatic decreases in thyroid hormones following resuscitation indicate a significant acute serum hypothyroid state that may benefit from L-T₄ treatment. L-T₄ enhances systemic oxygen consumption and delivery and these changes may contribute to l-T₄'s neural protective effect.