Document Detail


The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration.
MedLine Citation:
PMID:  17351059     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Reopening the injured lung with deep inflation (DI) and positive end-expiratory pressure (PEEP) likely depends on the duration and severity of acute lung injury (ALI), key features of which include increased alveolar permeability and fibrin accumulation. We hypothesized that the response to DI and PEEP would worsen as ALI evolves and that this would correspond with increasing accumulation of alveolar fibrin. C57BL/6 mice were anesthetized and aspirated 75 microl of HCl (pH 1.8) or buffered normal saline. Subgroups were reanesthetized 4, 14, 24, and 48 h later. Following DI, tissue damping (G) and elastance (H) were measured periodically at PEEP of 1, 3, and 6 cmH(2)O, and air within the lung (thoracic gas volume) was quantified by microcomputed tomography. Following DI, G and H increased with time during progressive lung derecruitment, the latter confirmed by microcomputed tomography. The rise in H was greater in acid-injured mice than in controls (P < 0.05) and also increased from 4 to 48 h after acid aspiration, reflecting progressively worsening injury. The rise in H was reduced by PEEP, but this effect was significantly blunted by 48 h (P < 0.05), also confirmed by thoracic gas volume. Lung permeability and alveolar fibrin also increased over the 48-h study period, accompanied by increasing levels and transcription of the fibrinolysis inhibitor plasminogen activator inhibitor-1. Lung injury worsens progressively in mice during the 48 h following acid aspiration. This injury manifests as progressively increasing alveolar instability, likely due to surfactant dysfunction caused by increasing levels of alveolar protein and fibrin.
Authors:
Gilman B Allen; Timothy Leclair; Mary Cloutier; John Thompson-Figueroa; Jason H T Bates
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-03-09
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  292     ISSN:  1040-0605     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2007 Jun 
Date Detail:
Created Date:  2007-06-11     Completed Date:  2007-07-27     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L1580-9     Citation Subset:  IM    
Affiliation:
Vermont Lung Center, Department of Medicine, University of Vermont, Burlington, Vermont, USA. Gil.Allen@uvm.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Markers / metabolism
Bronchoalveolar Lavage Fluid
Disease Models, Animal*
Disease Progression
Female
Fibrin / metabolism*
Fibrinolysis / physiology
Hydrochloric Acid / pharmacology
Lung Volume Measurements
Mice
Mice, Inbred C57BL*
Pneumonia, Aspiration / metabolism,  pathology*,  therapy
Positive-Pressure Respiration
Respiratory Distress Syndrome, Adult / metabolism,  pathology*,  therapy
Severity of Illness Index
Grant Support
ID/Acronym/Agency:
K08HL074107/HL/NHLBI NIH HHS; P20RR15557/RR/NCRR NIH HHS; R01 HL75593/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 7647-01-0/Hydrochloric Acid; 9001-31-4/Fibrin

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


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