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Effect of ventilation strategy and surfactant on inflammation in experimental pneumonia

¹ Dept of Anesthesiology, Erasmus-MC Faculty, Rotterdam, and ² Dept of Neonatology, Emma Children's Hospital, ³ Dept of Pulmonology, and ⁴ Laboratory of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands, and ⁵ Dept of Paediatrics, University of Lübeck, Lübeck, Germany.

CORRESPONDENCE: A. H. L. C. van Kaam, Dept of Neonatology (Room H3-150), Emma Children's Hospital Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DD, Amsterdam, The Netherlands. Fax: 31 206965099. E-mail: a.h.vankaam@amc.uva.nl

Keywords: Group B streptococcus, interleukin-8, lung protective ventilation, myeloperoxidase, surfactant, tumour necrosis factor-

Received: December 17, 2004
Accepted March 3, 2005

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 cmH₂O, 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)- 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-.

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.