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unknown
On the pulmonary toxicity of oxygen : III. The induction of oxygen dependency by oxygen use
Authors
Abdel-Latif
Allen
+76 more
Ambrus
Balentine
Barach
Blumenthal
Bolande
Chang
Chess
Claireaux
Cogswell
Collard
Cools
Crompton
Cross
D. Radford Shanklin
Da-Silva
deMello
Downs
Egan
Egan
Egan
Egan
Egan
Fisher
Frank
Frank
Gregory
Han
Hardin
Higgins
Ingalls
Jonxis
Kaarteenaho-Wiik
Kelly
Kwan
Langley
Le Floch
Lyra
Martin
McGrath
Morken
Morley
Mortoloa
Moss
Nash
Nishiki
Northway
Northway
Northway
Orzalesi
Petrou
Phillips
Robertson
Rudolph
Sahn
Schock
Schwartz
Scopes
Shanklin
Shanklin
Shanklin
Shanklin
Shanklin
Shanklin
Shanklin
Shanklin
Shanklin
Shanklin
Shanklin
Shanklin
Shanklin
Sunderam
Taylor
te Pas
Turrens
Urschitz
Winternitz
Publication date
1 May 2010
Publisher
'Elsevier BV'
Doi
Cite
Abstract
Author Posting. © The Author(s), 2010. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Experimental and Molecular Pathology 89 (2010): 36-45, doi:10.1016/j.yexmp.2010.05.004.Oxygen is central to the development of neonatal lung injury. The increase in oxygen exposure of the neonatal lung during the onset of extrauterine air breathing is an order of magnitude, from a range of 10-12 to 110-120 Torr. The contributions of oxygen and the volume and pressure relationships of ventilatory support to lung injury are not easily distinguished in the clinical setting. Sequential changes in inspired air or 100% oxygen were studied in 536 newborn rabbits without ventilatory support. Bilateral cervical vagotomies (BCV) were performed at 24 hours post natal to induce ventilatory distress which eventuates in hyaline membrane disease. The sequences applied yielded evidence for an induced state of oxygen dependency from oxygen use which was reflected in differences in survival and the extent of pulmonary injury. The median survival for animals kept in air throughout was 3 hours. Oxygen before vagotomy or during the first 3 hours afterwards extended the survival significantly but produced more extensive, more severe, and more rapid lung lesions. Returning animals to air after prior oxygen exposure reduced the number of survivors past 10 hours and shortened the maximum survival in those groups. These features indicate the development of a dependency of the defense mechanisms on the availability of oxygen at the higher level for metabolic and possibly other aspects of the pulmonary and systemic response to injury, beyond the usual physiological need. Subset analysis revealed additive and latent effects of oxygen and demonstrated a remarkable rapidity in onset of severe lesions under some circumstances, illustrating the toxicity of oxygen per se.John A. Hartford Foundation, New York, N.Y. 10022-171
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