Inhaled hydrogen sulfide protects against ventilator-induced lung injury.

摘要: Background Mechanical ventilation still causes an unacceptably high rate of morbidity and mortality because ventilator-induced lung injury (VILI). Therefore, new therapeutic strategies are needed to treat VILI. Hydrogen sulfide can induce hypothermia suspended animation-like states in mice. also confer antiinflammatory antiapoptotic effects. This study investigates the organ-protective effects inhaled hydrogen during mechanical ventilation. Methods Mice were ventilated with a tidal volume 12 ml/kg body weight for 6 h synthetic air absence or presence (80 parts per million) and, second series, at either mild normothermia. Staining sections determined degree damage by VILI score apoptotic cells. Bronchoalveolar lavage fluid was analyzed cytokines interleukin-1beta macrophage inflammatory protein-1beta neutrophil accumulation. Heme oxygenase-1 heat shock protein 70 expression assessed tissue Western immunoblot analysis. Results both normothermia led profound development VILI, characterized pulmonary edema, increased apoptosis, cytokine release, recruitment, up-regulation stress proteins such as heme 70. In contrast, application prevented edema formation, proinflammatory production, accumulation, inhibited expression. Conclusions Inhalation protects against inhibition responses. confers protection independently its ability