Triiodothyronine increases survival in canine hemorrhagic shock.

The euthyroid sick (low T3) syndrome occurs in shock and could influence survival. To evaluate the potential therapeutic value of triiodothyronine (T3) in circulatory collapse, 26 anesthetized, heparinized mongrel dogs were bled rapidly into a reservoir until mean arterial blood pressure (MAP) = 40 mmHg. After 60 min of hypotension, the animals were given 15 micrograms/kg of T3 i.v. (13 dogs) or an equal volume of normal saline (13 dogs), and the reservoir line was clamped for 30 min (uncompensated shock). The shed blood was then reinfused over 30 min. After 1 h of monitoring the dogs were returned to the kennel and observed for 3 days. T3 (15 micrograms/kg) or normal saline was administered i.v. on each of the first 3 postshock days. T3 administration caused significant increases during uncompensated shock in cardiac output, stroke volume, mean arterial pressure, right and left ventricular stroke work and systemic vascular resistance, with a decrease in pulmonary vascular resistance. Shortly after reinfusion of shed blood, hemodynamic values were similar in T3 and untreated animals. In the control group, 6 of 13 dogs died. However, only one of 13 T3 dogs died (P less than 0.05). Although the mechanism by which T3 enhances shock survival was not clearly identified, T3 might exert beneficial effects via the hypothalamic-pituitary-thyroid axis or by acting on cardiovascular receptors to improve hemodynamic function at a critical stage of shock. Additional studies of T3 therapy in clinical shock appear warranted.