Oxygen attenuates atelectasis-induced injury in the in vivo rat lung.
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.
Duggan
Michelle
M
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.
McNamara
Patrick J
PJ
Engelberts
Doreen
D
Pace-Asciak
Cecil
C
Babyn
Paul
P
Post
Martin
M
Kavanagh
Brian P
BP
D000818:Animals; D002199:Capillary Permeability; D003971:Diastole / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005652:Functional Residual Capacity; D006976:Hypertension, Pulmonary / Q000517:prevention & control*; D000860:Hypoxia / Q000150:complications; D008168:Lung / Q000098:blood supply*; D008297:Male; D010100:Oxygen / Q000494:pharmacology*; D011453:Prostaglandins / Q000502:physiology; D011651:Pulmonary Artery / Q000187:drug effects; D001261:Pulmonary Atelectasis / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley
D011453:Prostaglandins; D010100:Oxygen