HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 106/2/662    most recent 91109.2008v1 Submit a response View responses Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Allen, B. W. Articles by Piantadosi, C. A. Search for Related Content PubMed PubMed Citation Articles by Allen, B. W. Articles by Piantadosi, C. A.

REVIEW

HIGHLIGHTED TOPIC
The Physiology and Pathophysiology of the Hyperbaric and Diving Environments

Two faces of nitric oxide: implications for cellular mechanisms of oxygen toxicity

¹Center for Hyperbaric Medicine and Environmental Physiology, ²Department of Anesthesiology, and ³Division of Pulmonary Medicine, Department of Medicine, Duke University Medical Center, Durham, North Carolina; and ⁴Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia

ABSTRACT

Recent investigations have elucidated some of the diverse roles played by reactive oxygen and nitrogen species in events that lead to oxygen toxicity and defend against it. The focus of this review is on toxic and protective mechanisms in hyperoxia that have been investigated in our laboratories, with an emphasis on interactions of nitric oxide (NO) with other endogenous chemical species and with different physiological systems. It is now emerging from these studies that the anatomical localization of NO release, which depends, in part, on whether the oxygen exposure is normobaric or hyperbaric, strongly influences whether toxicity emerges and what form it takes, for example, acute lung injury, central nervous system excitation, or both. Spatial effects also contribute to differences in the susceptibility of different cells in organs at risk from hyperoxia, especially in the brain and lungs. As additional nodes are identified in this interactive network of toxic and protective responses, future advances may open up the possibility of novel pharmacological interventions to extend both the time and partial pressures of oxygen exposures that can be safely tolerated. The implications of a better understanding of the mechanisms by which NO contributes to central nervous system oxygen toxicity may include new insights into the pathogenesis of seizures of diverse etiologies. Likewise, improved knowledge of NO-based mechanisms of pulmonary oxygen toxicity may enhance our understanding of other types of lung injury associated with oxidative or nitrosative stress.

superoxide; superoxide dismutase 3; neurogenic pulmonary edema

This article has been cited by other articles:

				D. P. D'Agostino, D. G. Colomb Jr., and J. B. Dean Effects of hyperbaric gases on membrane nanostructure and function in neurons J Appl Physiol, March 1, 2009; 106(3): 996 - 1003. [Abstract] [Full Text] [PDF]

				D. R. Pendergast and C. E. G. Lundgren The physiology and pathophysiology of the hyperbaric and diving environments J Appl Physiol, January 1, 2009; 106(1): 274 - 275. [Full Text] [PDF]