α-Trinositol decreases lung edema formation after smoke inhalation in an ovine model

Inhalation injury is a dominant cause of mortality in thermally injured individuals. After acute lung injury induced by smoke inhalation, lung lymph flow (Q̇L) increased and pulmonary microvascular reflection coefficient to protein (σ) decreased, α-Trinositol (PP56, 1D-myo-inositol 1,2,6- trisphosphate) can decrease edema formation after thermal injury. We therefore tested the hypothesis that α-trinositol could decrease the pulmonary edema noted with inhalation injury. Seven days after surgical preparation, sheep were insufflated with smoke from burning cotton towels. The α-trinositol group (n = 8) were treated with α-trinositol (2 mg/kg + 3.5 mg · kg^-1 · h^-1). The sham group (n = 7) received an equal volume of 0.9% NaCl. The sham group showed a large increase in Q̇L (9.3 ± 1.7 to 54.1 ± 8.8 ml/h) and a decrease in σ (0.79 ± 0.03 to 0.48 ± 0.03) 24 h after smoke inhalation. α-Trinositol attenuated the increase in Q̇L (8.1 ± 1.2 to 25.6 ± 6.9 ml/h) and the decrease in σ (0.76 ± 0.03 to 0.60 ± 0.03) noted with smoke inhalation. α-Trinositol thus decreased the changes in pulmonary microvascular permeability and transvascular fluid flux noted with inhalation injury.