To examine whether reverse triiodothyronine (rT3), generally considered devoid of biological activity, could influence outcome in circulatory collapse, 23 anesthetized mongrel dogs were subjected to hemorrhagic shock. In 10 dogs, 15 μg/kg of rT3were administered in 30 min before hemorrhage. In 13 other dogs, an equal volume of saline was injected. The dogs were bled rapidly to a mean arterial pressure of 40 mm Hg, and after 60 min the reservoir line was clamped for 30 min. The shed blood was then reinfused over 30 min. After one hour of hemodynamic monitoring, the dogs were returned to the kennel and observed for at least 3 days. During shock there were few significant intergroup hemodynamic-metabolic differences. In the control group, six of 13 dogs died, whereas nine of ten dogs given rT3died (p< .03). This study strongly suggests that rT3exerts detrimental biological activity in canine hemorrhagic shock, Hence, rT3may play a causative role in the euthyroid sick (“low T3”) syndrome.