title: Protective ventilation to reduce inflammatory injury from one lung ventilation in a piglet model.
abstract: OBJECTIVE
  To test the hypothesis that protective ventilation strategy (PVS) as defined by the use of low stretch ventilation (tidal volume of 5 ml x kg(-1) and employing 5 cm of positive end expiratory pressure (PEEP) during one lung ventilation (OLV) in piglets would result in reduced injury compared to a control group of piglets who received the conventional ventilation (tidal volume of 10 ml x kg(-1) and no PEEP).
  
  
  BACKGROUND
  PVS has been found to be beneficial in adults to minimize injury from OLV. We designed the current study to test the beneficial effects of PVS in a piglet model of OLV.
  
  
  METHODS
  Ten piglets each were assigned to either 'Control' group (tidal volume of 10 ml x kg(-1) and no PEEP) or 'PVS' group (tidal volume of 5 ml x kg(-1) during the OLV phase and PEEP of 5 cm of H2O throughout the study). Experiment consisted of 30 min of baseline ventilation, 3 h of OLV, and again 30 min of bilateral ventilation. Respiratory parameters and proinflammatory markers were measured as outcome.
  
  
  RESULTS
  There was no difference in PaO2 between groups. PaCO2 (P < 0.01) and ventilatory rate (P < 0.01) were higher at 1.5 h OLV and at the end point in the PVS group. Peak inflating pressure (PIP) and pulmonary resistance were higher (P < 0.05) in the control group at 1.5 h OLV. tumor necrosis factor-alpha (P < 0.04) and IL-8 were less (P < 0.001) in the plasma from the PVS group, while IL-6 and IL-8 were less (P < 0.04) in the lung tissue from ventilated lungs in the PVS group.
  
  
  CONCLUSIONS
  Based on this model, PVS decreases inflammatory injury both systemically and in the lung tissue with no adverse effect on oxygenation, ventilation, or lung function.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Alfred I. duPont Hospital for Children, Wilmington, DE 19803, USA. mtheroux@nemours.org
authors.forename: Mary C
authors.initials: MC
authors.lastname: Theroux
authors.forename: Alicia O
authors.initials: AO
authors.lastname: Fisher
authors.forename: Liana M
authors.initials: LM
authors.lastname: Horner
authors.forename: Maria E
authors.initials: ME
authors.lastname: Rodriguez
authors.forename: Andrew T
authors.initials: AT
authors.lastname: Costarino
authors.forename: Thomas L
authors.initials: TL
authors.lastname: Miller
authors.forename: Thomas H
authors.initials: TH
authors.lastname: Shaffer
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D008168:Lung / Q000378:metabolism; D011014:Pneumonia / Q000150:complications / Q000517:prevention & control*; D011175:Positive-Pressure Respiration / Q000379:methods*; D012121:Respiration, Artificial / Q000009:adverse effects; D013552:Swine; D013990:Tidal Volume; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014655:Vascular Resistance; D055397:Ventilator-Induced Lung Injury / Q000209:etiology / Q000517:prevention & control*
chemical_list: D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha