title: Mechanical ventilation with lower tidal volumes and positive end-expiratory pressure prevents pulmonary inflammation in patients without preexisting lung injury.
abstract: BACKGROUND
  Mechanical ventilation with high tidal volumes aggravates lung injury in patients with acute lung injury or acute respiratory distress syndrome. The authors sought to determine the effects of short-term mechanical ventilation on local inflammatory responses in patients without preexisting lung injury.
  
  
  METHODS
  Patients scheduled to undergo an elective surgical procedure (lasting > or = 5 h) were randomly assigned to mechanical ventilation with either higher tidal volumes of 12 ml/kg ideal body weight and no positive end-expiratory pressure (PEEP) or lower tidal volumes of 6 ml/kg and 10 cm H2O PEEP. After induction of anesthesia and 5 h thereafter, bronchoalveolar lavage fluid and/or blood was investigated for polymorphonuclear cell influx, changes in levels of inflammatory markers, and nucleosomes.
  
  
  RESULTS
  Mechanical ventilation with lower tidal volumes and PEEP (n = 21) attenuated the increase of pulmonary levels of interleukin (IL)-8, myeloperoxidase, and elastase as seen with higher tidal volumes and no PEEP (n = 19). Only for myeloperoxidase, a difference was found between the two ventilation strategies after 5 h of mechanical ventilation (P < 0.01). Levels of tumor necrosis factor alpha, IL-1alpha, IL-1beta, IL-6, macrophage inflammatory protein 1alpha, and macrophage inflammatory protein 1beta in the bronchoalveolar lavage fluid were not affected by mechanical ventilation. Plasma levels of IL-6 and IL-8 increased with mechanical ventilation, but there were no differences between the two ventilation groups.
  
  
  CONCLUSIONS
  The use of lower tidal volumes and PEEP may limit pulmonary inflammation in mechanically ventilated patients without preexisting lung injury. The specific contribution of both lower tidal volumes and PEEP on the protective effects of the lung should be further investigated.
authors.affiliation: Department of Intensive Care Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. e.k.wolthuis@amc.uva.nl
authors.forename: Esther K
authors.initials: EK
authors.lastname: Wolthuis
authors.forename: Goda
authors.initials: G
authors.lastname: Choi
authors.forename: Mark C
authors.initials: MC
authors.lastname: Dessing
authors.forename: Paul
authors.initials: P
authors.lastname: Bresser
authors.forename: Rene
authors.initials: R
authors.lastname: Lutter
authors.forename: Misa
authors.initials: M
authors.lastname: Dzoljic
authors.forename: Tom
authors.initials: T
authors.lastname: van der Poll
authors.forename: Margreeth B
authors.initials: MB
authors.lastname: Vroom
authors.forename: Markus
authors.initials: M
authors.lastname: Hollmann
authors.forename: Marcus J
authors.initials: MJ
authors.lastname: Schultz
mesh_terms: D000368:Aged; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008171:Lung Diseases / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D008875:Middle Aged; D011014:Pneumonia / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D011175:Positive-Pressure Respiration / Q000379:methods*; D012121:Respiration, Artificial / Q000379:methods*; D013990:Tidal Volume / Q000502:physiology*
chemical_list: D018836:Inflammation Mediators