Hyperoxia may have attenuated pulmonary and systemic inflammation by compensating regional pulmonary hypoxia as well as tissue hypoxia resulting from chest trauma-induced hypoxemia: hypoxic hypoxia (FiO2 0.1) of incremental duration caused a time-dependent increase of the BAL fluid neutrophil count and albumin content reflecting alveolar-capillary leakage [64], and further aggravated endotoxin-induced ALI [65]. This evidence concerns the gene ALB and acute respiratory distress syndrome.