Hyperoxia-induced lung injury is characterized by an influx of inflammatory cells, increased pulmonary permeability, endothelial and epithelial cell death. This review highlights the mechanistic aspects of inflammation, vascular leak and cell death. The focus will be on agents that contribute to hyperoxia-induced lung injury in developmentally appropriate animal models, and those that have been detected in human premature neonates.
Division of Perinatal Medicine, Yale University School of Medicine, Department of Pediatrics, 333 Cedar Street, LCI 401B, New Haven, CT 06520-8064, USA
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