Oxygen toxicity and tolerance.

摘要: Normobaric oxygen toxicity is well described in all animal species. However susceptibility to exposure highly variable according age, species and strains. Similarly humans, prolonged high reported induce cough, shortness of breath, decrease vital capacity increase alveolo-capillary permeability. The toxic FIO2 threshold (length level) still debated. In patients with previous lung injury, this even more difficult delineate as pathologic pulmonary lesions might result from hyperoxia or primary insult. Oxygen free-radicals play a key role the pathophysiology toxicity. resistance tolerance obtained intraperitoneal, intravenous intratracheal endotoxin cytokines administration. Previous concentration also survival rate models. Protection may rely on antioxidant enzymes synthesis, nitric oxide production, neutrophils recruitment modulation alveolar macrophages activity. be suspected through several clinical studies reporting favorable outcome after long term-oxygen exposure. Better knowledge risks important re-evaluate goals mechanical ventilation (FIO2, SaO2, PEEP) and/or develop treatments prevent (surfactant, enzymes).