title: The pulmonary immune effects of mechanical ventilation in patients undergoing thoracic surgery.
abstract: Mechanical ventilation (MV) may induce an inflammatory alveolar response. One-lung ventilation (OLV) with tidal volumes (Vt) as used during two-lung ventilation is a suggested algorithm but may impose mechanical stress of the dependent lung and potentially aggravate alveolar mediator release. We studied whether ventilation with different Vt modifies pulmonary immune function, hemodynamics, and gas exchange. Thirty-two patients undergoing open thoracic surgery were randomized to receive either MV with Vt = 10 mL/kg (n = 16) or Vt = 5 mL/kg (n = 16) adjusted to normal Pa(CO2) during and after OLV. Fiberoptic bronchoalveolar lavage of the ventilated lung was performed, and cells, protein, tumor necrosis factor (TNF)-alpha, interleukin (IL)-8, soluble intercellular adhesion molecule (sICAM)-1, IL-10, and elastase were determined in the bronchoalveolar lavage. Data were analyzed by parametric or nonparametric tests, as indicated. In all patients, an increase of proinflammatory variables was found. The time courses of intra-alveolar cells, protein, albumin, IL-8, elastase, and IL-10 did not differ between the groups after OLV and postoperatively. TNF-alpha (8.4 versus 5.0 microg/mL) and sICAM-1 (52.7 versus 27.5 microg/mL) concentrations were significantly smaller after OLV with Vt = 5 mL/kg. These results indicate that MV may induce epithelial damage and a proinflammatory response in the ventilated lung. Reduction of tidal volume during OLV may reduce alveolar concentrations of TNF-alpha and of sICAM-1.
  
  
  CONCLUSIONS
  Reductions of tidal volume, with subsequently decreased peak airway pressures, may reduce some alveolar inflammatory responses seen with mechanical ventilation.
authors.affiliation: *Department of Anesthesiology and Intensive Care Medicine, †Department of Cardiovascular and Thoracic Surgery, ‡Institute of Immunology, and §Department of Cardiology, Angiology, and Pneumology, Otto-von-Guericke-University, Magdeburg, Germany.
authors.forename: Thomas
authors.initials: T
authors.lastname: Schilling
authors.forename: Alf
authors.initials: A
authors.lastname: Kozian
authors.forename: Christof
authors.initials: C
authors.lastname: Huth
authors.forename: Frank
authors.initials: F
authors.lastname: Bühling
authors.forename: Moritz
authors.initials: M
authors.lastname: Kretzschmar
authors.forename: Tobias
authors.initials: T
authors.lastname: Welte
authors.forename: Thomas
authors.initials: T
authors.lastname: Hachenberg
mesh_terms: D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D019272:Leukocyte Elastase / Q000032:analysis; D008168:Lung / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012121:Respiration, Artificial; D019616:Thoracic Surgical Procedures; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D019272:Leukocyte Elastase