Document Detail

Maintaining end-expiratory transpulmonary pressure prevents worsening of ventilator-induced lung injury caused by chest wall constriction in surfactant-depleted rats.
MedLine Citation:
PMID:  20890197     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To see whether in acute lung injury 1) compression of the lungs caused by thoracoabdominal constriction degrades lung function and worsens ventilator-induced lung injury; and 2) maintaining end-expiratory transpulmonary pressure by increasing positive end-expiratory pressure reduces the deleterious effects of chest wall constriction.
DESIGN: Experimental study in rats.
SETTING: Physiology laboratory.
INTERVENTIONS: Acute lung injury was induced in three groups of nine rats by saline lavage. Nine animals immediately killed served as a control group. Group L had lavage only, group LC had the chest wall constricted with an elastic binder, and group LCP had the same chest constriction but with positive end-expiratory pressure raised to maintain end-expiratory transpulmonary pressure. After lavage, all groups were ventilated with the same pattern for 1½ hrs.
MEASUREMENTS AND MAIN RESULTS: Transpulmonary pressure, measured with an esophageal balloon catheter, lung volume changes, arterial blood gasses, and pH were assessed during mechanical ventilation. Lung wet-to-dry ratio, albumin, tumor necrosis factor-α, interleukin-1β, interleukin-6, interleukin-10, and macrophage inflammatory protein-2 in serum and bronchoalveolar lavage fluid and serum E-selectin and von Willebrand Factor were measured at the end of mechanical ventilation. Lavage caused hypoxemia and acidemia, increased lung resistance and elastance, and decreased end-expiratory lung volume. With prolonged mechanical ventilation, lung mechanics, hypoxemia, and wet-to-dry ratio were significantly worse in group LC. Proinflammatory cytokines except E-selectin were elevated in serum and bronchoalveolar lavage fluid in all groups with significantly greater levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in group LC, which also exhibited significantly worse bronchiolar injury and greater heterogeneity of airspace expansion at a fixed transpulmonary pressure than other groups.
CONCLUSIONS: Chest wall constriction in acute lung injury reduces lung volume, worsens hypoxemia, and increases pulmonary edema, mechanical abnormalities, proinflammatory mediator release, and histologic signs of ventilator-induced lung injury. Maintaining end-expiratory transpulmonary pressure at preconstriction levels by adding positive end-expiratory pressure prevents these deleterious effects.
Stephen H Loring; Matteo Pecchiari; Patrizia Della Valle; Ario Monaco; Guendalina Gentile; Edgardo D'Angelo
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Critical care medicine     Volume:  38     ISSN:  1530-0293     ISO Abbreviation:  Crit. Care Med.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-22     Completed Date:  2010-12-21     Revised Date:  2014-04-23    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2358-64     Citation Subset:  AIM; IM    
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MeSH Terms
Analysis of Variance
Bronchoalveolar Lavage Fluid / chemistry
Constriction, Pathologic
Disease Models, Animal
Disease Progression
Positive-Pressure Respiration / methods*
Primary Prevention / methods
Pulmonary Gas Exchange
Pulmonary Surfactants / metabolism*
Random Allocation
Reference Values
Respiratory Mechanics
Statistics, Nonparametric
Thoracic Wall
Tidal Volume
Ventilator-Induced Lung Injury / physiopathology*,  therapy*
Grant Support
Reg. No./Substance:
0/Pulmonary Surfactants
Comment In:
Crit Care Med. 2010 Dec;38(12):2418-9   [PMID:  21088512 ]

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

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