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Published ahead of print on February 20, 2004, doi:10.1164/rccm.200312-1779OC

Am. J. Respir. Crit. Care Med., Volume 169, Number 9, May 2004, 1046-1053

A more recent version of this article appeared on May 1, 2004
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Submitted on December 30, 2003
Accepted on February 20, 2004

Reducing Atelectasis Attenuates Bacterial Growth and Translocation in Experimental Pneumonia

Anton H van Kaam1*, Robert A Lachmann2, Egbert Herting3, Anne De Jaegere2, Freek van Iwaarden4, L. Arnold Noorduyn5, Joke H Kok6, Jack J Haitsma2, and Burkhard Lachmann2

1 Department of Anesthesiology, Erasmus-MC Faculty, Rotterdam, The Netherlands; Department of Neonatology, Emma Children's Hospital AMC, Amsterdam, The Netherlands, 2 Department of Anesthesiology, Erasmus-MC Faculty, Rotterdam, The Netherlands, 3 Department of Pediatrics, University of Gottingen, Gottingen, Germany, 4 Laboratory of Pediatrics, Erasmus-MC Faculty, Rotterdam, The Netherlands, 5 Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands, 6 Department of Neonatology, Emma Children's Hospital AMC, Amsterdam, The Netherlands

* To whom correspondence should be addressed. E-mail: a.h.vankaam{at}amc.uva.nl.

Besides being one of the mechanisms responsible for ventilator-induced lung injury, atelectasis also seems to aggravate the course of experimental pneumonia. In this study, we examined the effect of reducing the degree of atelectasis by natural modified surfactant and/or open lung ventilation, on bacterial growth and translocation in a piglet model of group B streptococcal pneumonia. After creating surfactant-deficiency by whole lung lavage, intratracheal instillation of bacteria induced severe pneumonia with bacterial translocation into the blood stream, resulting in a mortality rate of almost 80%. Treatment with 300 mg/kg exogenous surfactant prior to instillation of streptococci, attenuated both bacterial growth and translocation, and prevented clinical deterioration. This goal was also achieved by reversing atelectasis in lavaged animals via open lung ventilation. Combining both exogenous surfactant and open lung ventilation, prevented bacterial translocation completely, comparable to group B streptococci instillation into healthy animals. We conclude that exogenous surfactant and open lung ventilation attenuate bacterial growth and translocation in experimental pneumonia and that this attenuation is at least in part mediated by a reduction in atelectasis. These findings suggest that minimizing alveolar collapse by exogenous surfactant and open lung ventilation may reduce the risk of pneumonia and subsequent sepsis in ventilated patients.


Key words: open lung ventilation, atelectasis, sepsis




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