Document Detail


Different ventilation strategies affect lung function but do not increase tumor necrosis factor-alpha and prostacyclin production in lavaged rat lungs in vivo.
MedLine Citation:
PMID:  10598628     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Using an in vivo animal model of surfactant deficiency, the authors compared the effect of different ventilation strategies on oxygenation and inflammatory mediator release from the lung parenchyma. METHODS: In adult rats that were mechanically ventilated with 100% oxygen, acute lung injury was induced by repeated lung lavage to obtain an arterial oxygen partial pressure < 85 mmHg (peak pressure/positive end-expiratory pressure [PEEP] = 26/6 cm H2O). Animals were then randomly assigned to receive either exogenous surfactant therapy, partial liquid ventilation, ventilation with high PEEP (16 cm H2O), ventilation with low PEEP (8 cm H2O), or ventilation with an increase in peak inspiratory pressure (to 32 cm H2O; PEEP = 6 cm H2O). Two groups of healthy nonlavaged rats were ventilated at a peak pressure/PEEP of 32/6 and 32/0 cm H2O, respectively. Blood gases were measured. Prostacyclin (PGI2) and tumor necrosis factor-alpha (TNF-alpha) concentrations in serum and bronchoalveolar lavage fluid (BALF) as well as protein concentration in BALF were determined after 90 and 240 min and compared with mechanically ventilated and spontaneously breathing controls. RESULTS: Surfactant, partial liquid ventilation, and high PEEP improved oxygenation and reduced BALF protein levels. Ventilation with high PEEP at high mean airway pressure levels increased BALF PGI2 levels, whereas there was no difference in BALF TNF-alpha levels between groups. Serum PGI2 and TNF-alpha levels did not increase as a result of mechanical ventilation when compared with those of spontaneously breathing controls. CONCLUSIONS: Although alveolar protein concentration and oxygenation markedly differed with different ventilation strategies in this model of acute lung injury, there were no indications of ventilation-induced systemic PGI2 and TNF-alpha release, nor of pulmonary TNF-alpha release. Mechanical ventilation at high mean airway pressure levels increased PGI2 levels in the bronchoalveolar lavage-accessible space.
Authors:
S J Verbrugge; S Uhlig; S J Neggers; C Martin; H D Held; J J Haitsma; B Lachmann
Related Documents :
333078 - The effect of independent variations in inspiratory-expiratory ratio and end expiratory...
7035518 - Optimal endexpiratory airway pressure for ventilated patients.
12615628 - Positive end-expiratory pressure after a recruitment maneuver prevents both alveolar co...
324318 - Pulmonary wedge catheterization during positive end-expiratory pressure ventilation in ...
8363948 - The epidemiology of pressure sores.
20233378 - High hydrostatic pressure and the cell membrane: stress response of saccharomyces cerev...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Anesthesiology     Volume:  91     ISSN:  0003-3022     ISO Abbreviation:  Anesthesiology     Publication Date:  1999 Dec 
Date Detail:
Created Date:  1999-12-30     Completed Date:  1999-12-30     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  1300217     Medline TA:  Anesthesiology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1834-43     Citation Subset:  AIM; IM    
Affiliation:
Department of Anesthesiology, Erasmus University Rotterdam, The Netherlands.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
6-Ketoprostaglandin F1 alpha / blood,  metabolism
Animals
Bronchoalveolar Lavage Fluid / chemistry
Carbon Dioxide / blood
Epoprostenol / biosynthesis*
Irrigation
Lung / metabolism*,  physiology*
Male
Oxygen / blood
Proteins / metabolism
Pulmonary Alveoli / metabolism
Rats
Rats, Sprague-Dawley
Respiration, Artificial*
Respiratory Function Tests
Tumor Necrosis Factor-alpha / biosynthesis*
Chemical
Reg. No./Substance:
0/Proteins; 0/Tumor Necrosis Factor-alpha; 124-38-9/Carbon Dioxide; 35121-78-9/Epoprostenol; 58962-34-8/6-Ketoprostaglandin F1 alpha; 7782-44-7/Oxygen

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


Previous Document:  Exposure to cigarette smoke impairs alveolar macrophage functions during halothane and isoflurane an...
Next Document:  Tissue factor expression in vital organs during murine traumatic shock: role of transcription factor...