Show simple item record

dc.contributor.authorShanklin, D. Radford  Concept link
dc.date.accessioned2010-07-07T12:42:05Z
dc.date.available2010-07-07T12:42:05Z
dc.date.issued2010-05
dc.identifier.urihttps://hdl.handle.net/1912/3724
dc.descriptionAuthor 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.en_US
dc.description.abstractOxygen 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.en_US
dc.description.sponsorshipJohn A. Hartford Foundation, New York, N.Y. 10022-1713en_US
dc.format.mimetypeapplication/pdf
dc.language.isoen_USen_US
dc.relation.urihttps://doi.org/10.1016/j.yexmp.2010.05.004
dc.subjectOxygen toxicityen_US
dc.subjectLung injuryen_US
dc.subjectMetabolic dependencyen_US
dc.subjectRespiratory distress syndromeen_US
dc.subjectHyaline membrane diseaseen_US
dc.subjectBilateral cervical vagotomyen_US
dc.subjectAnimal models for human diseaseen_US
dc.subjectSemi-log graphicsen_US
dc.subjectArea under the curve analysisen_US
dc.titleOn the pulmonary toxicity of oxygen : III. The induction of oxygen dependency by oxygen useen_US
dc.typePreprinten_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record