The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration.

The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration. Research Abstract Details 

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The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration. Abstract Text:

Gilman B Allen,Timothy Leclair,Mary Cloutier,John Thompson-Figueroa,Jason H T Bates,

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.

The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration. Publishing Authors By Initials

GB Allen,T Leclair,M Cloutier,J Thompson-Figueroa,JH Bates,

For similar investigative techniques: epidemiologic methods: data collection: health surveys: health status indicators: severity of illness index research abstracts see: investigative techniques: epidemiologic methods: data collection: health surveys: health status indicators: severity of illness index research

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The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Lung cellular and

VOLUME: 292

Page Numbers: L1580-9

Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

ISSN: 1040-0605

DAY: 9

MONTH: 03

YEAR: 2007

The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901229

The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration. Keywords Mesh Terms:

KEYWORDS: Severity of Illness Index

MESH TERMS: therapy

Chemical & Substance for Abstract: The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration. Information

Substance Name: Fibrin

Registry Number: 9001-31-4

Grant and Affiliation Information for The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration.

AFFILIATION: Vermont Lung Center, Department of Medicine, University of Vermont, Burlington, Vermont, USA. Gil.Allen@uvm.edu

Country: United States

AGENCY: United States NHLBI

GRANT: R01 HL75593

ACRONYM: HL

MEDLINETA: Am J Physiol Lung Cell Mol Phy

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