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

X. Q. Yuan, C. H. Shatney, D. S. Dewitt, D. S. Prough, R. A. Smith

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)720-725
Number of pages6
JournalAmerican Surgeon
Issue number12
StatePublished - 1988
Externally publishedYes

ASJC Scopus subject areas

  • Surgery


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