Triiodothyronine (T3) improves cardiovascular function during hemorrhagic shock.

Prior work showed that an intact thyroid axis augments survival from hemorrhagic shock (HS); this study assesses the effects of specific thyroid-related hormones on cardiovascular (CV) function during HS. Following thyroidectomy, 32 conditioned male dogs were subjected to HS to a mean arterial pressure (MAP) of 60 mm Hg for 90 min then to 40 mm Hg for 30 min. Postshock (PS), the dogs received thyroid-releasing hormone (TRH; 2 mg/kg), thyroid-stimulating hormone [control (TSH; 10 IU)], T3 (12 micrograms/kg), or T4 (40 micrograms/kg). Thirty minutes following treatment (PTX), they were resuscitated with shed blood and 50 ml/kg saline. CV and hormonal parameters were measured PS, PTX, postresuscitation (PR), and on day 2 (D2). There were no PS differences in CV parameters between groups. Following treatment, T3 significantly increased MAP (59.0 +/- 13 vs, 39.9 +/- 2.2 mm Hg) and cardiac output (CO; 0.92 +/- 0.1 vs. 0.80 +/- 0.1 liter/min; P < 0.05 by ANOVA). TRH treatment significantly improved PTX MAP (62.7 +/- 10 vs. 40.8 +/- 2.1; P < 0.05 by ANOVA). TSH and T4 did not significantly change PTX MAP or CO. There were no significant CV differences in the four groups following resuscitation or on D2. In conclusion, T3 improves MAP and CO during hemorrhagic shock. TRH transiently improved PTX blood pressure. Further study of the mechanism of this beneficial response afforded by T3 administration is warranted.