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1.5. Objective of this study Moriuchi et al. have developed a model of the decrease in PaO2 induced by a low dose 15 l kg ; oleic acid for the screening of a drug for hypoxemia with pulmonary vascular permeability.46-48 ; However, the precise mechanism of the lung injury has not been elucidated. In recent years, it is reported that ROSs play an important role in the oleic acid-induced lung injury, 7 ; especially neutrophil-mediated superoxides.12 ; However, detailed investigations have not been carried out on sources for ROS other than neutrophil such as pulmonary endothelial cells and alveolar epithelial cells, and changes in antioxidant systems in the lungs. Therefore, the objectives of this study are to examine 1 ; oxidative changes in the lung injury induced by oleic acid using bronchoalveolar fluid BALF ; biomarkers, and assess whether or not NADPH oxidase and or xanthine oxidase contribute to ROSs generation in the lung injury Chapter 2 ; , 2 ; effect of PMNs depletion on the oxidative changes and hypoxemia in the lung injury Chapter 3 ; , 3 ; whether or not pulmonary artery endothelial cells and or alveolar epithelial cells generate ROSs by oleic acid, whether or not a possible resource of ROSs released from the cells is an NADPH oxidase-like enzyme, and whether or not the intra-cellular ROSs cause cell death Chapter 4 ; , 4 ; changes in ATP content in the lungs injured by the injection of oleic acid, and whether phosphoenolpyruvate, an intermediate substance of glycolysis which can carry an energy into cells, attenuates hypoxemia and pulmonary vascular.
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