| Alterations to surfactant precede physiological deterioration during high tidal volume ventilation. | |
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MedLine Citation:
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PMID: 18344412 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Lung injury due to mechanical ventilation is associated with an impairment of endogenous surfactant. It is unknown whether this impairment is a consequence of or an active contributor to the development and progression of lung injury. To investigate this issue, the present study addressed three questions: Do alterations to surfactant precede physiological lung dysfunction during mechanical ventilation? Which components are responsible for surfactant's biophysical dysfunction? Does exogenous surfactant supplementation offer a physiological benefit in ventilation-induced lung injury? Adult rats were exposed to either a low-stretch [tidal volume (Vt) = 8 ml/kg, positive end-expiratory pressure (PEEP) = 5 cmH2O, respiratory rate (RR) = 54-56 breaths/min (bpm), fractional inspired oxygen (Fi(O2)) = 1.0] or high-stretch (Vt = 30 ml/kg, PEEP = 0 cmH2O, RR = 14-16 bpm, Fi(O2) = 1.0) ventilation strategy and monitored for either 1 or 2 h. Subsequently, animals were lavaged and the composition and function of surfactant was analyzed. Separate groups of animals received exogenous surfactant after 1 h of high-stretch ventilation and were monitored for an additional 2 h. High stretch induced a significant decrease in blood oxygenation after 2 h of ventilation. Alterations in surfactant pool sizes and activity were observed at 1 h of high-stretch ventilation and progressed over time. The functional impairment of surfactant appeared to be caused by alterations to the hydrophobic components of surfactant. Exogenous surfactant treatment after a period of high-stretch ventilation mitigated subsequent physiological lung dysfunction. Together, these results suggest that alterations of surfactant are a consequence of the ventilation strategy that impair the biophysical activity of this material and thereby contribute directly to lung dysfunction over time. |
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Authors:
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Adam A Maruscak; Daniel W Vockeroth; Brandon Girardi; Tanya Sheikh; Fred Possmayer; James F Lewis; Ruud A W Veldhuizen |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-03-14 |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 294 ISSN: 1040-0605 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2008 May |
Date Detail:
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Created Date: 2008-05-02 Completed Date: 2008-06-30 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L974-83 Citation Subset: IM |
Affiliation:
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Lawson Health Research Institute F4-117, 268 Grosvenor St., London, ON, Canada, N6A 4V2. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure Cholesterol / metabolism Disease Models, Animal Interleukin-6 / metabolism Lung / metabolism Lung Diseases / etiology*, metabolism* Male Oxygen / blood Positive-Pressure Respiration / adverse effects* Pulmonary Surfactant-Associated Protein A / metabolism* Pulmonary Surfactant-Associated Protein B / metabolism* Rats Rats, Sprague-Dawley Tidal Volume* Tumor Necrosis Factor-alpha / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-6; 0/Pulmonary Surfactant-Associated Protein A; 0/Pulmonary Surfactant-Associated Protein B; 0/Tumor Necrosis Factor-alpha; 57-88-5/Cholesterol; 7782-44-7/Oxygen |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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