Journal article
Oxygen attenuates atelectasis-induced injury in the in vivo rat lung
Anesthesiology (Philadelphia), Vol.103(3), pp.522-531
2005
DOI: 10.1097/00000542-200509000-00015
PMID: 16129977
Abstract
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.
Details
- Title: Subtitle
- Oxygen attenuates atelectasis-induced injury in the in vivo rat lung
- Creators
- Michelle DUGGAN - Department of Pediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, CanadaPatrick J MCNAMARA - Department of Pediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, CanadaDoreen ENGELBERTS - Program in Lung Biology, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, CanadaCecil PACE-ASCIAK - Program in Integrative Biology, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, CanadaPaul BABYN - Department of Radiology, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, CanadaMartin POST - Programs in Lung and Integrative Biology, The Research Institute, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, CanadaBrian P KAVANAGH - Programs in Lung and Integrative Biology, The Research Institute, Departments of Critical Care Medicine and Anaesthesia, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada
- Resource Type
- Journal article
- Publication Details
- Anesthesiology (Philadelphia), Vol.103(3), pp.522-531
- Publisher
- Lippincott
- DOI
- 10.1097/00000542-200509000-00015
- PMID
- 16129977
- ISSN
- 0003-3022
- eISSN
- 1528-1175
- Language
- English
- Date published
- 2005
- Academic Unit
- Stead Family Department of Pediatrics; Neonatology; Internal Medicine
- Record Identifier
- 9984093315902771
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