Triiodothyronine (T₃) antagonizes adverse effects of high circulating reverse-T₃ (rT₃) during hemorrhagic shock

To examine whether triiodothyronine (T₃) could counteract the lethal effect of exogenous reverse T₃ (rT₃) in hemorrhagic shock, 21 anesthetized, heparinized mongrel dogs were given 15 μg/kg of rT₃ IV. Thirty minutes later, the dogs were bled rapidly into a reservoir to achieve and maintain a mean arterial pressure of 40 mm Hg. After 60 minutes at 40 mm Hg (compensated shock), the reservoir line was clamped for 30 minutes (uncompensated shock). The shed blood was then reinfused over 30 minutes, and the dogs were monitored for an additional 60 minutes. At the start of uncompensated shock, 11 dogs were given at least 15 μg/kg of T₃ IV, and 10 animals received saline. Before T₃ treatment, there were no significant intergroup differences in the measured hemodynamic and blood gas variables. In the untreated group, 8 of 10 dogs (80%) died during uncompensated shock, in comparison to 3 of 11 dogs (27%) that received T₃ (P < 0.01). Long-term survival in the T₃ group was 5/11 (45%), significantly higher than that (1/10, 10%) in the untreated group (P < 0.05). These results, interpreted in relationship to previous studies, suggest that the therapeutic efficacy of T₃ in canine hemorrhagic shock may be related to antagonism of adverse effects of endogenous rT₃.