Pulmonary oxygen toxicity.
Although oxygen therapy has been used in the care of critically ill patients for many years, the recognition of pulmonary oxygen toxicity as an important clinical problem is relatively recent. The biochemical basis of oxygen toxicity is increased production of highly reactive, partially reduced metabolites of oxygen, including hydrogen peroxide and free radicals, by cells in hyperoxia. Enzymatic intracellular defense mechanisms exist which protect cells from the toxic effects of oxygen free radicals. The physiologic manifestations of oxygen toxicity include decreases in vital capacity, diffusing capacity, and lung compliance. The pathologic changes of oxygen toxicity are not specific and resemble those of the adult respiratory distress syndrome. Many drugs used in the care of patients, including bleomycin, nitrofurantoin, and corticosteroids, may exacerbate oxygen-induced lung injury. No effective pharmacologic means exist for lessening pulmonary oxygen toxicity in humans.
D004361:Drug Tolerance; D005609:Free Radicals; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008171:Lung Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D010100:Oxygen / Q000378:metabolism / Q000633:toxicity*; D010101:Oxygen Consumption; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000473:pathology; D012129:Respiratory Function Tests; D014797:Vital Capacity
D005609:Free Radicals; D006861:Hydrogen Peroxide; D010100:Oxygen