title: One-lung ventilation with high tidal volumes and zero positive end-expiratory pressure is injurious in the isolated rabbit lung model.
abstract: We tested the hypothesis that one-lung ventilation (OLV) with high tidal volumes (VT) and zero positive end-expiratory pressure (PEEP) may lead to ventilator-induced lung injury. In an isolated, perfused rabbit lung model, VT and PEEP were set to avoid lung collapse and overdistension in both lungs, resulting in a straight pressure-time (P-vs-t) curve during constant flow. Animals were randomized to (a) nonprotective OLV (left lung) (n = 6), with VT values as high as before randomization and zero PEEP; (b) protective OLV (left lung) (n = 6), with 50% reduction of VT and maintenance of PEEP as before randomization; and (c) control group (n = 6), with ventilation of two lungs as before randomization. The nonprotective OLV was associated with significantly smaller degrees of collapse and overdistension in the ventilated lung (P < 0.001). Peak inspiratory pressure values were higher in the nonprotective OLV group (P < 0.001) and increased progressively throughout the observation period (P < 0.01). The mean pulmonary artery pressure and lung weight gain values, as well as the concentration of thromboxane B(2), were comparatively higher in the nonprotective OLV group (P < 0.05). A ventilatory strategy with VT values as high as those used in the clinical setting and zero PEEP leads to ventilator-induced lung injury in this model of OLV, but this can be minimized with VT and PEEP values set to avoid lung overdistension and collapse.
  
  
  CONCLUSIONS
  One-lung ventilation with high tidal volumes and zero positive end-expiratory pressure (PEEP) is injurious in the isolated rabbit lung model. A ventilatory strategy with tidal volumes and PEEP set to avoid lung overdistension and collapse minimizes lung injury during one-lung ventilation in this model.
authors.affiliation: Clinic of Anesthesiology and Intensive Care Medicine, University Clinic Carl Gustav Carus, Technical University Dresden, Germany. mgabreu@aol.com
authors.forename: Marcelo
authors.initials: M
authors.lastname: Gama de Abreu
authors.forename: Manuel
authors.initials: M
authors.lastname: Heintz
authors.forename: Axel
authors.initials: A
authors.lastname: Heller
authors.forename: Roswitha
authors.initials: R
authors.lastname: Széchényi
authors.forename: Detlev Michael
authors.initials: DM
authors.lastname: Albrecht
authors.forename: Thea
authors.initials: T
authors.lastname: Koch
mesh_terms: D000403:Airway Resistance / Q000502:physiology; D000465:Algorithms; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002406:Catheterization, Peripheral; D005260:Female; D055370:Lung Injury; D009929:Organ Size / Q000187:drug effects; D011175:Positive-Pressure Respiration; D011651:Pulmonary Artery; D011817:Rabbits; D012121:Respiration, Artificial / Q000009:adverse effects*; D015656:Respiratory Mechanics; D013929:Thromboxane B2 / Q000097:blood; D013990:Tidal Volume / Q000502:physiology*
chemical_list: D013929:Thromboxane B2