Pulmonary biophysical effects of triiodothyronine augmentation during sepsis-induced hypothyroidism

Sepsis may cause pulmonary dysfunction and altered metabolism; triiodothyronine (T3) replacement improves lung function and surfactant pool. We evaluated the biophysical effects of T3 replacement during sepsis-induced hypothyroidism. Male Holtzman rats underwent cecal ligation and puncture (CLP) or sham laparotomy (S); treatment was administered consisting of T3 (3 ng/h) or saline. Twenty-four hours after CLP, lungs were ventilation-perfused with oxygenated N-2-hydroxylpiperazine-N1-2-ethanesulfonic acid (HEPES) with 5 microCi 3-H choline (3-HC) for 1 hour. Perfusion pressures were continuously monitored; perfusate was monitored for 3-HC uptake and oxygen extraction. Triiodothyronine treatment abolished the sepsis-induced decrease in free T3 levels (S = 68 +/- 5 ng/dL, CLP < 15 ng/dL, CLP/T3 = 91 +/- 20 ng/dL). Lung wet-to-dry ratios and vascular and tracheal pressures were maintained by T3 treatment. Choline incorporation was not altered by sepsis or treatment. Triiodothyronine treatment reduced the sepsis-induced increase in oxygen requirement and improved septic pulmonary compromise through a nonhypermetabolic effect.