Similar but not the same: normobaric and hyperbaric pulmonary oxygen toxicity, the role of nitric oxide

Physiol 293: L229–L238, 2007. First published April 6, 2007; doi:10.1152/ajplung.00450.2006.—Pulmonary manifestations of oxy-gen toxicity were studied and quantified in rats breathing98 % O2 at 1, 1.5, 2, 2.5, and 3 ATA to test our hypothesis that different patterns of pulmonary injury would emerge, reflecting a role for central nervous system (CNS) excitation by hyperbaric oxygen. At 1.5 atmosphere absolute (ATA) and below, the well-recognized pattern of diffuse pulmonary damage developed slowly with an extensive in-flammatory response and destruction of the alveolar-capillary barrier leading to edema, impaired gas exchange, respiratory failure, and death; the severity of these effects increased with time over the 56-h period of observation. At higher inspired O2 pressures, 2–3 ATA, pulmonary injury was greatly accelerated but less inflammatory in character, and events in the brain were a prelude to a distinct lung pathology. The CNS-mediated component of this lung injury could b