title: Hyperoxia in the intensive care unit: why more is not always better.
abstract: OBJECTIVE
  Hyperoxic inspired gas is essential for patients with hypoxic respiratory failure; it is also suspected, however, as a contributor to the pathogenesis of acute lung injury. Several recent studies in humans, animals, and cell culture have identified mechanisms by which hyperoxia may exert deleterious effects on critically ill patients. This review identifies relevant new findings regarding hyperoxic lung injury in the context of providing guidance for future clinical studies.
  
  
  RESULTS
  Recent studies have clarified the roles of both receptor-mediated and mitochondrial cell death pathways in experimental hyperoxic lung injury. Studies in animals demonstrate that hyperoxia interacts with mechanical stretch to augment ventilator-induced lung injury. Finally, studies in humans implicate hyperoxia in impairment of host defense responses to infections.
  
  
  CONCLUSIONS
  Although hyperoxia has not been conclusively identified as a clinically important cause of lung injury in humans, animal data strongly implicate it. Reports of interaction effects between hyperoxia and both mechanical ventilation and host defense suggest that clinical studies of hyperoxia must take these variables into account. Accumulating data about how hyperoxia initiates cell death provide guidance for development of both biomarkers to identify hyperoxia-induced injury and pharmacological interventions to limit hyperoxia's adverse effects.
authors.affiliation: Department of Medicine, University of Washington, Seattle, Washington 98195-6522, USA. billa@u.washington.edu
authors.forename: William A
authors.initials: WA
authors.lastname: Altemeier
authors.forename: Scott E
authors.initials: SE
authors.lastname: Sinclair
mesh_terms: D000818:Animals; D017209:Apoptosis; D006801:Humans; D018496:Hyperoxia / Q000150:complications*; D007362:Intensive Care Units; D010100:Oxygen / Q000009:adverse effects* / Q000627:therapeutic use; D017382:Reactive Oxygen Species; D012121:Respiration, Artificial; D012128:Respiratory Distress Syndrome / Q000209:etiology; D012131:Respiratory Insufficiency / Q000628:therapy*; D012307:Risk Factors
chemical_list: D017382:Reactive Oxygen Species; D010100:Oxygen