THYROID-HORMONE LOSS AND REPLACEMENT DURING RESUSCITATION FROM CARDIAC-ARREST IN DOGS

Circulating concentrations of thyroxine (T4), triiodothyronine (T3), a nd reverse triiodothyronine (rT3) were followed in dogs subjected to 9 min of normothermic ventricular fibrillation. Significant decreases w ere detected 12 h post-arrest when compared to pre-arrest levels in to tal T4 (P < 0.0005), free T4 (P < 0.0005), total T3 (P < 0.003), and f ree T3 (P < 0.003), and levels of reverse T3 were significantly elevat ed (P = 0.0001). Similar changes occurred with only 30 s of arrest. Po st-arrest replacement therapy with 7.5 mug/kg per h (Rx-7.5) and 15 mu g/kg per h (Rx-15) levothyroxine sodium (L-T4) increased total T4, fre e T4, and total T3 (P < 0.01). Free T3 decreased in the Rx-7.5 group ( P < 0.01) and did not fall in the Rx-15 group (P = 0. 16). Reverse T3 increased with either treatment (P < 0.005). Both treatment groups had higher levels of all five hormones than non-treated animals (P < 0.00 1). Neurologic function, assessed with a standardized scoring system, showed significant improvement in the treated groups by 6 h (P < 0.05, compared to non-treated group) and remained significant through 24 h post-arrest (P < 0.05). The documentation of rapid and dramatic change s in thyroid hormones immediately following cardiac arrest and resusci tation indicates a significant acute hypothyroid state that may potent ially benefit from replacement therapy.