title: Effects of positive end-expiratory pressure titration and recruitment maneuver on lung inflammation and hyperinflation in experimental acid aspiration-induced lung injury.
abstract: BACKGROUND
  In acute lung injury positive end-expiratory pressure (PEEP) and recruitment maneuver are proposed to optimize arterial oxygenation. The aim of the study was to evaluate the impact of such a strategy on lung histological inflammation and hyperinflation in pigs with acid aspiration-induced lung injury.
  
  
  METHODS
  Forty-seven pigs were randomly allocated in seven groups: (1) controls spontaneously breathing; (2) without lung injury, PEEP 5 cm H2O; (3) without lung injury, PEEP titration; (4) without lung injury, PEEP titration + recruitment maneuver; (5) with lung injury, PEEP 5 cm H2O; (6) with lung injury, PEEP titration; and (7) with lung injury, PEEP titration + recruitment maneuver. Acute lung injury was induced by intratracheal instillation of hydrochloric acid. PEEP titration was performed by incremental and decremental PEEP from 5 to 20 cm H2O for optimizing arterial oxygenation. Three recruitment maneuvers (pressure of 40 cm H2O maintained for 20 s) were applied to the assigned groups at each PEEP level. Proportion of lung inflammation, hemorrhage, edema, and alveolar wall disruption were recorded on each histological field. Mean alveolar area was measured in the aerated lung regions.
  
  
  RESULTS
  Acid aspiration increased mean alveolar area and produced alveolar wall disruption, lung edema, alveolar hemorrhage, and lung inflammation. PEEP titration significantly improved arterial oxygenation but simultaneously increased lung inflammation in juxta-diaphragmatic lung regions. Recruitment maneuver during PEEP titration did not induce additional increase in lung inflammation and alveolar hyperinflation.
  
  
  CONCLUSIONS
  In a porcine model of acid aspiration-induced lung injury, PEEP titration aimed at optimizing arterial oxygenation, substantially increased lung inflammation. Recruitment maneuvers further improved arterial oxygenation without additional effects on inflammation and hyperinflation.
authors.affiliation: Department of Surgery, Laboratory of Medical Investigation/Anesthesiology (LIM/08)-Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
authors.forename: Aline M
authors.initials: AM
authors.lastname: Ambrosio
authors.forename: Rubin
authors.initials: R
authors.lastname: Luo
authors.forename: Denise T
authors.initials: DT
authors.lastname: Fantoni
authors.forename: Claudia
authors.initials: C
authors.lastname: Gutierres
authors.forename: Qin
authors.initials: Q
authors.lastname: Lu
authors.forename: Wen-Jie
authors.initials: WJ
authors.lastname: Gu
authors.forename: Denise A
authors.initials: DA
authors.lastname: Otsuki
authors.forename: Luiz M S
authors.initials: LM
authors.lastname: Malbouisson
authors.forename: Jose O C
authors.initials: JO
authors.lastname: Auler
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Rouby
mesh_terms: D000818:Animals; D005260:Female; D006851:Hydrochloric Acid / Q000008:administration & dosage / Q000009:adverse effects; D055370:Lung Injury / Q000139:chemically induced / Q000473:pathology* / Q000628:therapy*; D011014:Pneumonia / Q000139:chemically induced / Q000473:pathology* / Q000628:therapy*; D011175:Positive-Pressure Respiration / Q000379:methods*; D011897:Random Allocation; D011999:Recruitment, Neurophysiological / Q000502:physiology*; D015656:Respiratory Mechanics / Q000502:physiology; D013552:Swine
chemical_list: D006851:Hydrochloric Acid