Document Detail


Ventilator-induced lung injury leads to loss of alveolar and systemic compartmentalization of tumor necrosis factor-alpha.
MedLine Citation:
PMID:  11126266     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: To determine the effect on compartmentalization of the tumor necrosis factor (TNF)-alpha response in the lung and systemically after ventilation with high peak inspiratory pressure with and without positive end-expiratory pressure (PEEP). DESIGN AND SETTING: Prospective, randomized, animal study in an experimental laboratory of a university. SUBJECTS AND INTERVENTIONS: 85 male Sprague-Dawley rats. Lipopolysaccharide was given intratracheally or intraperitoneally to stimulate TNF-alpha production; control animals received a similar amount of saline. Animals were subsequently ventilated for 20 min in a pressure control mode with peak inspiratory pressure/PEEP ratio of either 45/0 or 45/10 (frequency 30 bpm, I/E ratio 1:2, FIO2 = 1). MEASUREMENTS AND RESULTS: Blood gas tension and arterial pressures were recorded at 1, 10, and 20 min after start of mechanical ventilation. After killing of the animals pressure-volume curves were recorded, and bronchoalveolar lavage (BAL) was performed for assessment of protein content and the small/large surfactant aggregate ratio. TNF-alpha was determined in serum and BAL. TNF-alpha levels were significantly increased after lipopolysaccharide stimulation; furthermore ventilation without PEEP resulted in a significant shift of TNF-alpha to the nonstimulated compartment as opposed to ventilation with a PEEP level of 10 cmH2O. CONCLUSIONS: Ventilation strategies which are known to induce ventilation-induced lung injury (VILI) disturb the compartmentalization of the early cytokines response in the lung and systemically. Furthermore, the loss of compartmentalization is a two-way disturbance, with cytokines shifting from the vascular side to the alveolar side and vice versa. A ventilation strategy (PEEP level of 10 cmH2O) which prevents VILI significantly diminished this shift in cytokines.
Authors:
J J Haitsma; S Uhlig; R Göggel; S J Verbrugge; U Lachmann; B Lachmann
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Intensive care medicine     Volume:  26     ISSN:  0342-4642     ISO Abbreviation:  Intensive Care Med     Publication Date:  2000 Oct 
Date Detail:
Created Date:  2000-12-20     Completed Date:  2001-02-15     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7704851     Medline TA:  Intensive Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1515-22     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology, Erasmus University Rotterdam, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Blood Gas Analysis
Blood Pressure
Bronchoalveolar Lavage Fluid / chemistry
Disease Models, Animal*
Inflammation
Lipopolysaccharides
Male
Positive-Pressure Respiration / adverse effects*,  methods
Prospective Studies
Pulmonary Alveoli / chemistry*
Random Allocation
Rats
Rats, Sprague-Dawley
Respiratory Distress Syndrome, Adult / etiology*,  metabolism*,  physiopathology
Tidal Volume
Time Factors
Tumor Necrosis Factor-alpha / analysis*,  metabolism*
Chemical
Reg. No./Substance:
0/Lipopolysaccharides; 0/Tumor Necrosis Factor-alpha
Comments/Corrections
Comment In:
Intensive Care Med. 2001 Feb;27(2):452   [PMID:  11396300 ]
Intensive Care Med. 2000 Oct;26(10):1411-3   [PMID:  11126249 ]

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


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