Document Detail


Physiologic, biochemical, and imaging characterization of acute lung injury in mice.
MedLine Citation:
PMID:  15894601     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
RATIONALE: Most models of acute lung injury in mice have yet to be fully characterized.
OBJECTIVES: To directly compare and contrast endotoxin and oleic acid models of acute lung injury in mice in terms of their physiologic, biochemical, histopathologic, and imaging manifestations.
METHODS: Survival studies, lung weights, x-ray computed tomographic scanning, light and electron microscopy, bronchoalveolar lavage, lung uptake of ((18)F)fluorodeoxyglucose, tissue myeloperoxidase, arterial blood gases, mean arterial pressure, and lung tissue prostanoids were measured in separate groups of C57Bl/6 mice (normal animals, endotoxin only [20 microg/g], oleic acid only [0.15 microl/g], or endotoxin + oleic acid).
RESULTS: Endotoxin alone caused only mild pulmonary neutrophilic inflammation with little functional or structural damage to the alveolar architecture. In contrast, oleic acid caused severe alveolar damage with the development of alveolar edema of the increased-permeability type with associated abnormalities in gas exchange. When given together, endotoxin and oleic acid acted synergistically to increase pulmonary edema and to worsen gas exchange and hemodynamics, thereby increasing mortality. This synergism was significantly attenuated by the prior administration of the endotoxin antagonist E5564 (eritoran).
CONCLUSIONS: Under the conditions of these studies, only mice exposed to oleic acid showed both structural and functional characteristics of acute lung injury. Nevertheless, endotoxin had potent synergistic physiologic effects that increased mortality. Overall, these models, which can be translated to genetically altered mice, are amenable to study with state-of-the-art imaging techniques, and with experimental interventions that can probe the underlying mechanisms of injury.
Authors:
Zhaohui Zhou; James Kozlowski; Daniel P Schuster
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.     Date:  2005-05-13
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  172     ISSN:  1073-449X     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-07-25     Completed Date:  2005-09-27     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  344-51     Citation Subset:  AIM; IM    
Affiliation:
Department of Internal Medicine and Radiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bronchoalveolar Lavage
Disease Models, Animal
Drug Synergism
Endotoxins / administration & dosage
Fluorodeoxyglucose F18 / diagnostic use
Mice
Mice, Inbred C57BL
Microscopy, Electron
Neutrophil Infiltration
Neutrophils / physiology
Oleic Acid / administration & dosage
Peroxidase / analysis
Positron-Emission Tomography / methods
Prostaglandins / analysis
Radiopharmaceuticals / diagnostic use
Respiratory Distress Syndrome, Adult / chemically induced,  diagnosis*,  metabolism*,  physiopathology,  radionuclide imaging
Tomography, X-Ray Computed
Grant Support
ID/Acronym/Agency:
EB04732/EB/NIBIB NIH HHS; HL32815/HL/NHLBI NIH HHS; HL52535/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Endotoxins; 0/Prostaglandins; 0/Radiopharmaceuticals; 112-80-1/Oleic Acid; 63503-12-8/Fluorodeoxyglucose F18; EC 1.11.1.7/Peroxidase
Comments/Corrections

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