Abstract
Prolonged exposure to elevated concentrations of oxygen causes extensive lung injury in all mammalian species studies to date1. Lung oxidant damage is characterized by alterations in the alveolo-capillary barrier which increases permeability to solutes and causes interstitial and alveolar edema leading to respiratory failure. These phenomena can be seen in patients with acute hypoxemic respiratory failure (AHRF) when airspace flooding occurs from damaged pulmonary vessels and alveolar membranes, thus interfering with oxygen transfer from the airspaces into the blood 2-4.
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