Document Detail

Endotoxin induces respiratory failure and increases surfactant turnover and respiration independent of alveolocapillary injury in rats.
MedLine Citation:
PMID:  12045126     Owner:  NLM     Status:  MEDLINE    
Although endotoxin-induced acute lung injury is associated with inflammation, alveolocapillary injury, surfactant dysfunction, and altered lung mechanics, the precise sequence of these changes is polemic. We have studied the early pathogenesis of acute lung injury in spontaneously breathing anesthetized rats after intravenous infusion of Salmonella abortus equi endotoxin. The animals became hypoxic, and airway resistance, tissue resistance, lung elastance, and static compliance all deteriorated well before any change in alveolar neutrophils, macrophages, lung fluid (99mTc-labeled diethylenetriamine pentaacetic acid), or 125I-albumin flux, which were only appreciably increased at 8.5 hours. Lung elastance deteriorated before airway resistance, indicating that the compliance change was specific rather than caused by reduced lung volume. The subcellular and alveolar content of surfactant proteins A and B, cholesterol, disaturated phospholipids, and phospholipid classes remained normal in the face of a dramatic increase in the synthesis and turnover of 3H-disaturated phosphatidylcholine. Our findings indicate that the increase in surfactant disaturated phospholipid turnover reflects, at least in part, an approximately five-fold increase in "sigh frequency." We suggest that endotoxin has direct effects on tissue resistance and lung elastance independent of surfactant composition and that the initial respiratory failure results primarily from endotoxin-induced ventilation/perfusion mismatch independent of edema or alveolocapillary injury per se.
Kate G Davidson; Andrew D Bersten; Heather A Barr; Kay D Dowling; Terence E Nicholas; Ian R Doyle
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  165     ISSN:  1073-449X     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  2002 Jun 
Date Detail:
Created Date:  2002-06-04     Completed Date:  2002-07-03     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1516-25     Citation Subset:  AIM; IM    
Department of Human Physiology, School of Medicine, Flinders University, South Australia, Australia.
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MeSH Terms
Airway Resistance / physiology
Blood Gas Analysis
Blood-Air Barrier / drug effects,  physiology*
Capillary Permeability / drug effects,  physiology
Disease Models, Animal
Endotoxins / pharmacology*
Lung / metabolism
Lung Injury
Pulmonary Surfactants / metabolism*
Rats, Sprague-Dawley
Reference Values
Respiratory Function Tests
Respiratory Insufficiency / physiopathology*
Respiratory Mechanics
Sensitivity and Specificity
Severity of Illness Index
Reg. No./Substance:
0/Endotoxins; 0/Pulmonary Surfactants

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

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