title: Relative roles of vascular and airspace pressures in ventilator-induced lung injury.
abstract: OBJECTIVE
  To determine whether elevations in pulmonary vascular pressure induced by mechanical ventilation are more injurious than elevations of pulmonary vascular pressure of similar magnitude occurring in the absence of mechanical ventilation.
  
  
  METHODS
  Prospective comparative laboratory investigation.
  
  
  METHODS
  University research laboratory.
  
  
  METHODS
  Male New Zealand white rabbits.
  
  
  METHODS
  Three groups of isolated, perfused rabbit lungs were exposed to cyclic elevation of pulmonary artery pressures arising from either intermittent positive pressure mechanical ventilation or from pulsatile perfusion of lungs held motionless by continuous positive airway pressure. Peak, mean, and nadir pulmonary artery pressures and mean airway pressure were matched between groups (35, 27.4 +/- 0.74, and 20.8 +/- 1.5 mm Hg, and 17.7 +/- 0.22 cm H2O, respectively).
  
  
  RESULTS
  Lungs exposed to elevated pulmonary artery pressures attributable to intermittent positive pressure mechanical ventilation formed more edema (6.8 +/- 1.3 vs. 1.1 +/- 0.9 g/g of lung), displayed more perivascular (61 +/- 26 vs. 15 +/- 13 vessels) and alveolar hemorrhage (76 +/- 11% vs. 26 +/- 18% of alveoli), and underwent larger fractional declines in static compliance (88 +/- 4.4% vs. 48 +/- 25.1% decline) than lungs exposed to similar peak and mean pulmonary artery pressures in the absence of tidal positive pressure ventilation.
  
  
  CONCLUSIONS
  Isolated phasic elevations of pulmonary artery pressure may cause less damage than those occurring during intermittent positive pressure mechanical ventilation, suggesting that cyclic changes in perivascular pressure surrounding extra-alveolar vessels may be important in the genesis of ventilator-induced lung injury.
authors.affiliation: Department of Pulmonary and Critical Care Medicine, Regions Hospital, University of Minnesota, St. Paul, MN, USA.
authors.forename: J R
authors.initials: JR
authors.lastname: Hotchkiss
authors.forename: L
authors.initials: L
authors.lastname: Blanch
authors.forename: A
authors.initials: A
authors.lastname: Naveira
authors.forename: A B
authors.initials: AB
authors.lastname: Adams
authors.forename: C
authors.initials: C
authors.lastname: Carter
authors.forename: D A
authors.initials: DA
authors.lastname: Olson
authors.forename: P H
authors.initials: PH
authors.lastname: Leo
authors.forename: J J
authors.initials: JJ
authors.lastname: Marini
mesh_terms: D000818:Animals; D006439:Hemodynamics; D055370:Lung Injury; D008297:Male; D011312:Pressure; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000209:etiology*; D011817:Rabbits; D012121:Respiration, Artificial / Q000009:adverse effects*