Hyperoxia Damages Cultured Endothelial Cells Causing Increased Neutrophil Adherence

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Abstract
Exposure of cultured bovine pulmonary artery endothelial cells to hyperoxia (95% O 2) caused cellular injury manifested by decreased growth rates and release of cytoplasmic lactic dehydrogenase (LDH). In addition, a greater number of polymorphonuclear leukocytes (PMN) adhered to endothelial cells that had been exposed to hyperoxia for 24 or 48 h than to control endothelial cells that had been exposed to normoxia (15% O 2). Direct endothelial cell injury from hyperoxia may contribute to vascular damage and the increased PMN accumulation seen in lungs of animals exposed to hyperoxia.