TY - JOUR
T1 - Effect of ventilation strategy and surfactant on inflammation in experimental pneumonia
AU - van Kaam, A. H.L.C.
AU - Lutter, R.
AU - Lachmann, R. A.
AU - Haitsma, J. J.
AU - Herting, E.
AU - Snoek, M.
AU - De Jaegere, A.
AU - Kok, J. H.
AU - Lachmann, B.
N1 - Copyright:
Copyright 2012 Elsevier B.V., All rights reserved.
PY - 2005/7
Y1 - 2005/7
N2 - This study explored, the inflammatory response during experimental pneumonia in surfactant-depleted animals as a function of ventilation strategies and surfactant treatment. Following intratracheal instillation of Group B streptococci (GBS), surfactant-depleted piglets were treated with conventional (positive-end expiratory pressure (PEEP) of 5 cmH 2O, tidal volume 7 mL·kg -1) or open lung ventilation. During the latter, collapsed alveoli were recruited by applying high peak inspiratory pressures for a short period of time, combined with high levels of PEEP and the smallest possible pressure amplitude. Subgroups in both ventilation arms also received exogenous surfactant. Conventionally ventilated healthy animals receiving GBS and surfactant-depleted animals receiving saline served as controls. In contrast with both control groups, surfactant-depleted animals challenged with GBS and conventional ventilation showed high levels of interleukin (IL)-8, tumour necrosis factor (TNF)-α and myeloperoxidase in bronchoalveolar lavage fluid after 5 h of ventilation. Open lung ventilation attenuated this inflammatory response, but exogenous surfactant did not. Systemic dissemination of the inflammatory response was minimal, as indicated by low serum levels of IL-8 and TNF-α. In conclusion, the current study indicates that the ventilation strategy, but not exogenous surfactant, is an important modulator of the inflammation during Group B streptococci pneumonia in mechanically ventilated surfactant-depleted animals.
AB - This study explored, the inflammatory response during experimental pneumonia in surfactant-depleted animals as a function of ventilation strategies and surfactant treatment. Following intratracheal instillation of Group B streptococci (GBS), surfactant-depleted piglets were treated with conventional (positive-end expiratory pressure (PEEP) of 5 cmH 2O, tidal volume 7 mL·kg -1) or open lung ventilation. During the latter, collapsed alveoli were recruited by applying high peak inspiratory pressures for a short period of time, combined with high levels of PEEP and the smallest possible pressure amplitude. Subgroups in both ventilation arms also received exogenous surfactant. Conventionally ventilated healthy animals receiving GBS and surfactant-depleted animals receiving saline served as controls. In contrast with both control groups, surfactant-depleted animals challenged with GBS and conventional ventilation showed high levels of interleukin (IL)-8, tumour necrosis factor (TNF)-α and myeloperoxidase in bronchoalveolar lavage fluid after 5 h of ventilation. Open lung ventilation attenuated this inflammatory response, but exogenous surfactant did not. Systemic dissemination of the inflammatory response was minimal, as indicated by low serum levels of IL-8 and TNF-α. In conclusion, the current study indicates that the ventilation strategy, but not exogenous surfactant, is an important modulator of the inflammation during Group B streptococci pneumonia in mechanically ventilated surfactant-depleted animals.
UR - http://www.scopus.com/inward/record.url?scp=21744435775&partnerID=8YFLogxK
U2 - 10.1183/09031936.05.00144504
DO - 10.1183/09031936.05.00144504
M3 - Journal articles
C2 - 15994397
AN - SCOPUS:21744435775
SN - 0903-1936
VL - 26
SP - 112
EP - 117
JO - European Respiratory Journal
JF - European Respiratory Journal
IS - 1
ER -