2007/04/06 by Demchenko It, Karen E. Welty‐Wolf, Barry W. Allen +1 · 1 citation
Neuroscience · Medicine · Biochemistry, Genetics and Molecular Biology · #Neuroscience of respiration and sleep #Cardiac Arrest and Resuscitation #Heme Oxygenase-1 and Carbon Monoxide #Nitric oxide #Oxygen toxicity #Lung #Pulmonary toxicity #Medicine #Anesthesia #Pulmonary edema #Toxicity #Nitric oxide synthase #Respiratory system #Pathology #Pharmacology #Internal medicine
paper · doi:10.1152/ajplung.00450.2006
openalex publication_date 2007/04/06 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
Pulmonary manifestations of oxygen toxicity were studied and quantified in rats breathing >98% O(2) 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 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 O(2) 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 be attenuated by selective inhibition of neuronal nitric oxide synthase (nNOS) or by unilateral transection of the vagus nerve. We propose that extrapulmonary, 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.