Document Detail


Oxygen attenuates atelectasis-induced injury in the in vivo rat lung.
MedLine Citation:
PMID:  16129977     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Atelectasis results in impaired compliance and gas exchange and, in extreme cases, increased microvascular permeability, pulmonary hypertension, and right ventricular dysfunction. It is not known whether such atelectasis-induced lung injury is due to the direct mechanical effects of lung volume reduction and alveolar collapse or due to the associated regional lung hypoxia. The authors hypothesized that addition of supplemental oxygen to an atelectasis-prone ventilation strategy would attenuate the pulmonary vascular effects and reduce the local levels of vasoconstrictor eicosanoids. METHODS: In series 1, anesthetized, atelectasis-prone mechanically ventilated rats were randomly assigned to one of six groups based on the inspired oxygen concentration and ventilated without recruitment. Series 2 was performed to determine the cardiac and pulmonary vascular effects of 21% versus 100% inspired oxygen. In series 3, computed tomography scans were performed after ventilation with a recruitment strategy (21% O2) or no recruitment strategy (21% O2 or 100% O2). In series 4, functional residual capacity was measured in animals where the gas was 21% or 100% O2. RESULTS: The partial pressure of arterial oxygen increased with increasing inspired oxygen, but the alveolar-arterial oxygenation gradient was also greater with higher inspired oxygen. Ventilation with 21% O2 (but not with 100% O2) was associated with progressive pulmonary vascular impedance and increased pulmonary vascular permeability. Prostaglandin F2alpha was increased by mechanical ventilation, especially without supplemental oxygen. Computed tomography scans demonstrated no atelectasis in recruited lungs, and atelectasis in nonrecruited lungs that was greater with supplemental oxygen. Increased atelectasis with 100% O2 (vs. 21% O2) was demonstrated by measurement of functional residual capacity. CONCLUSIONS: Although supplemental oxygen worsened atelectasis in this model, it prevented the pathologic effects of atelectasis, including microvascular leak and pulmonary hypertension. Atelectasis-induced lung injury seems to be mediated by hypoxia rather than by the direct mechanical effects of atelectasis.
Authors:
Michelle Duggan; Patrick J McNamara; Doreen Engelberts; Cecil Pace-Asciak; Paul Babyn; Martin Post; Brian P Kavanagh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Anesthesiology     Volume:  103     ISSN:  0003-3022     ISO Abbreviation:  Anesthesiology     Publication Date:  2005 Sep 
Date Detail:
Created Date:  2005-08-30     Completed Date:  2005-10-27     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  1300217     Medline TA:  Anesthesiology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  522-31     Citation Subset:  AIM; IM    
Affiliation:
Programs in Lung and Integrative Biology, The Research Institute, Department of Critical Care Medicine, The Hosptial for Sick Children and the University of Toronto, Ontario, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / complications
Capillary Permeability*
Diastole / drug effects
Dose-Response Relationship, Drug
Functional Residual Capacity
Hypertension, Pulmonary / prevention & control*
Lung / blood supply*
Male
Oxygen / pharmacology*
Prostaglandins / physiology
Pulmonary Artery / drug effects
Pulmonary Atelectasis / complications,  drug therapy*,  physiopathology
Rats
Rats, Sprague-Dawley
Chemical
Reg. No./Substance:
0/Prostaglandins; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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