Document Detail

Alterations to surfactant precede physiological deterioration during high tidal volume ventilation.
MedLine Citation:
PMID:  18344412     Owner:  NLM     Status:  MEDLINE    
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.
Adam A Maruscak; Daniel W Vockeroth; Brandon Girardi; Tanya Sheikh; Fred Possmayer; James F Lewis; Ruud A W Veldhuizen
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-03-14
Journal Detail:
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:
Created Date:  2008-05-02     Completed Date:  2008-06-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L974-83     Citation Subset:  IM    
Lawson Health Research Institute F4-117, 268 Grosvenor St., London, ON, Canada, N6A 4V2.
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MeSH Terms
Blood Pressure
Cholesterol / metabolism
Disease Models, Animal
Interleukin-6 / metabolism
Lung / metabolism
Lung Diseases / etiology*,  metabolism*
Oxygen / blood
Positive-Pressure Respiration / adverse effects*
Pulmonary Surfactant-Associated Protein A / metabolism*
Pulmonary Surfactant-Associated Protein B / metabolism*
Rats, Sprague-Dawley
Tidal Volume*
Tumor Necrosis Factor-alpha / metabolism
Reg. No./Substance:
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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