Thyroid hormone in neural rescue.

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 micrograms/kg/h = CA + 7.5 or 15 micrograms/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 micrograms/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.