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 micrograms/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 micrograms/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 less than 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 less than 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.