Hyperoxia damages cultured endothelial cells causing increased neutrophil adherence.
Exposure of cultured bovine pulmonary artery endothelial cells to hyperoxia (95% O2) 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% O2). Direct endothelial cell injury from hyperoxia may contribute to vascular damage and the increased PMN accumulation seen in lungs of animals exposed to hyperoxia.
D000818:Animals; D002417:Cattle; D002448:Cell Adhesion; D002455:Cell Division; D002478:Cells, Cultured; D004727:Endothelium / Q000166:cytology / Q000201:enzymology / Q000502:physiology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009504:Neutrophils / Q000502:physiology*; D010100:Oxygen / Q000633:toxicity*; D011651:Pulmonary Artery / Q000166:cytology*
D007770:L-Lactate Dehydrogenase; D010100:Oxygen