Comparison of different degrees of variability in tidal volume to prevent deterioration of respiratory system elastance in experimental acute lung inflammation.
BACKGROUND
Variable ventilation improves respiratory function, but it is not known whether the amount of variability in tidal volume (VT) can be reduced in recruited lungs without a deterioration of respiratory system elastance.


METHODS
Acute lung inflammation was induced by intratracheal instillation of lipopolysaccharide in 35 Wistar rats. Twenty-eight animals were anaesthetized and ventilated in volume-controlled mode. Lungs were recruited by random variation of VT (mean 6 ml kg(-1), coefficient of variation 30%, normal distribution) for 30 min. Animals were randomly assigned to different amounts of VT variability (n=7 for 90 min per group): 30, 15, 7.5, or 0%. Lung function, diffuse alveolar damage, and gene expression of biological markers associated with cell mechanical stress, inflammation, and fibrogenesis were assessed. Seven animals were not ventilated and served as controls for post-mortem analyses.


RESULTS
A VT variability of 30%, but not 15, 7.5, or 0%, prevented deterioration of respiratory system elastance [Mean (SD) -7.5 (8.7%), P<0.05; 21.1 (9.6%), P<0.05; 43.3 (25.9), P<0.05; and 41.2 (16.4), P<0.05, respectively]. Diffuse alveolar damage was lower with a VT variability of 30% than with 0% and without ventilation, because of reduced oedema and haemorrhage. A VT variability of 30, 15, or 7.5% reduced the gene expression of amphiregulin, cytokine-induced neutrophil chemoattractant-1, and tumour necrosis factor α compared with a VT variability of 0%.


CONCLUSIONS
In this model of acute lung inflammation, a VT variability of 30%, compared with 15 and 7.5%, was necessary to avoid deterioration of respiratory system elastance and was not associated with lung histological damage.
Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil.
T
T
Kiss
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil.
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PL
Silva
Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany.
R
R
Huhle
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil.
L
L
Moraes
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil.
R S
RS
Santos
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil.
N S
NS
Felix
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil.
C L
CL
Santos
Laboratory of Cellular and Molecular Physiology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil.
M M
MM
Morales
Department of Pathology, School of Medicine, University of São Paulo, São Paulo, Brazil.
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VL
Capelozzi
Institute of Anatomy, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany.
M
M
Kasper
Department of Surgical Sciences and Integrated Diagnostics, IRCCS AOU San Martino-IST, University of Genoa, Genoa, Italy.
P
P
Pelosi
Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany.
M
M
Gama de Abreu
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil prmrocco@gmail.com.
P R M
PR
Rocco
D000208:Acute Disease; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D008070:Lipopolysaccharides; D008297:Male; D010313:Partial Pressure; D011014:Pneumonia / Q000503:physiopathology* / Q000628:therapy; D011175:Positive-Pressure Respiration / Q000379:methods*; D011659:Pulmonary Gas Exchange / Q000502:physiology; D017208:Rats, Wistar; D015656:Respiratory Mechanics; D013990:Tidal Volume / Q000502:physiology*
D008070:Lipopolysaccharides; D002245:Carbon Dioxide
Escherichia coli; inflammation; inspiratory positive-pressure ventilation; mechanical ventilation; respiratory mechanics