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1 Center for Hyperbaric Medicine and Environmental Physiology, Duke University Medical Center, Durham, North Carolina, United States; Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina, United States; Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russian Federation
2 Center for Hyperbaric Medicine and Environmental Physiology, Duke University Medical Center, Durham, North Carolina, United States; Division of Pulmonary Medicine, Department of Medicine, Duke University Medical Center, United States
3 Center for Hyperbaric Medicine and Environmental Physiology, Duke University Medical Center, Durham, North Carolina, United States; Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina, United States
4 Center for Hyperbaric Medicine and Environmental Physiology, Duke University Medical Center, Durham, North Carolina, United States; Division of Pulmonary Medicine, Department of Medicine, Duke University Medical Center, United States; Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina, United States
* To whom correspondence should be addressed. E-mail: piant001{at}mc.duke.edu.
Pulmonary manifestations of oxygen toxicity were studied and quantified in rats breathing greater than 98% 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 CNS excitation by hyperbaric oxygen. At 1.5 ATA and below, the well-recognized pattern of diffuse pulmonary damage developed slowly with an extensive inflammatory 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 to 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 be attenuated by selective inhibition of neuronal nitric oxide synthase (nNOS) or by unilateral transection of the vagus nerve. We propose that extra-pulmonary, neurogenic events predominate in the pathogenesis of acute pulmonary oxygen toxicity in hyperbaric oxygenation, as nNOS activity drives lung injury by modulating the output of central autonomic pathways.
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