title: Pulmonary lesion induced by low and high positive end-expiratory pressure levels during protective ventilation in experimental acute lung injury.
abstract: OBJECTIVE
  To investigate the effects of low and high levels of positive end-expiratory pressure (PEEP), without recruitment maneuvers, during lung protective ventilation in an experimental model of acute lung injury (ALI).
  
  
  METHODS
  Prospective, randomized, and controlled experimental study.
  
  
  METHODS
  University research laboratory.
  
  
  METHODS
  Wistar rats were randomly assigned to control (C) [saline (0.1 mL), intraperitoneally] and ALI [paraquat (15 mg/kg), intraperitoneally] groups.
  
  
  RESULTS
  After 24 hours, each group was further randomized into four groups (six rats each) at different PEEP levels = 1.5, 3, 4.5, or 6 cm H2O and ventilated with a constant tidal volume (6 mL/kg) and open thorax. Lung mechanics [static elastance (Est, L) and viscoelastic pressure (DeltaP2, L)] and arterial blood gases were measured before (Pre) and at the end of 1-hour mechanical ventilation (Post). Pulmonary histology (light and electron microscopy) and type III procollagen (PCIII) messenger RNA (mRNA) expression were measured after 1 hour of mechanical ventilation. In ALI group, low and high PEEP levels induced a greater percentage of increase in Est, L (44% and 50%) and DeltaP2, L (56% and 36%) in Post values related to Pre. Low PEEP yielded alveolar collapse whereas high PEEP caused overdistension and atelectasis, with both levels worsening oxygenation and increasing PCIII mRNA expression.
  
  
  CONCLUSIONS
  In the present nonrecruited ALI model, protective mechanical ventilation with lower and higher PEEP levels than required for better oxygenation increased Est, L and DeltaP2, L, the amount of atelectasis, and PCIII mRNA expression. PEEP selection titrated for a minimum elastance and maximum oxygenation may prevent lung injury while deviation from these settings may be harmful.
authors.affiliation: Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, RJ, Brazil.
authors.forename: Caroline P
authors.initials: CP
authors.lastname: Pássaro
authors.forename: Pedro L
authors.initials: PL
authors.lastname: Silva
authors.forename: Andréia F
authors.initials: AF
authors.lastname: Rzezinski
authors.forename: Simone
authors.initials: S
authors.lastname: Abrantes
authors.forename: Viviane R
authors.initials: VR
authors.lastname: Santiago
authors.forename: Liliane
authors.initials: L
authors.lastname: Nardelli
authors.forename: Raquel S
authors.initials: RS
authors.lastname: Santos
authors.forename: Carolina M L
authors.initials: CM
authors.lastname: Barbosa
authors.forename: Marcelo M
authors.initials: MM
authors.lastname: Morales
authors.forename: Walter A
authors.initials: WA
authors.lastname: Zin
authors.forename: Marcelo B P
authors.initials: MB
authors.lastname: Amato
authors.forename: Vera L
authors.initials: VL
authors.lastname: Capelozzi
authors.forename: Paolo
authors.initials: P
authors.lastname: Pelosi
authors.forename: Patricia R M
authors.initials: PR
authors.lastname: Rocco
mesh_terms: D055371:Acute Lung Injury / Q000628:therapy*; D000818:Animals; D008171:Lung Diseases / Q000209:etiology; D011175:Positive-Pressure Respiration / Q000009:adverse effects* / Q000379:methods; D051381:Rats; D017208:Rats, Wistar