title: Hyperoxia exacerbates microvascular lung injury following acid aspiration.
abstract: OBJECTIVE
  To examine the effects of an increase in ambient oxygen (O2) concentrations on the extent of inflammatory pulmonary damage following acid aspiration.
  
  
  METHODS
  Prospective, controlled laboratory study.
  
  
  METHODS
  University-affiliated animal research facility.
  
  
  METHODS
  Male, Long Evans rats weighing 250 to 300 g.
  
  
  METHODS
  Rats were injured by instillation of 1.2 mL/kg normal saline solution/HCl, pH= 1.25 (acid), into the lungs via a tracheotomy. Animals were allowed to awaken and were exposed to 21%, 50%, or 98% O2 for 0 to 5 h (n/group > or = 10). In a separate set of experiments, injured rats exposed to 98% O2 were treated with different doses of deferoxamine, just prior to injury. Uninjured rats and rats injured with normal saline solution, pH = 5.3, were used as the control group.
  
  
  METHODS
  Injury was determined by assessing lung function (lung compliance and arterial blood gases) and alveolar-capillary wall integrity (wet/dry weight, lung albumin permeability index [PI], and intrapulmonary hemorrhage [HI]).
  
  
  RESULTS
  Intrapulmonary instillation of acid increased PI, HI, and decreased static lung compliance compared to uninjured control animals. Increased ambient oxygen following acid aspiration decreased lung compliance, 1.06+/-0.03 mL/kg/cm H2O, in oxygen-exposed lungs when compared to the lungs exposed to air, 1.26+/-0.04, following a low pH aspirate (p<0.05). An increase in protein leakage into the lung tissue was noted in oxygen-exposed animals, PI=1.33+/-0.10, vs air-exposed rats, 0.89+/-0.07 (p<0.05). The hyperoxia-induced increase in lung injury was prevented by 30 mg/kg or higher deferoxamine treatment, 0.78+/-0.05 (p<0.05). Exposure of animals to 98% O2 for 2 h was sufficient to produce the same increase in microvascular protein leakage as 5-h exposure to O2 following low pH aspirate.
  
  
  CONCLUSIONS
  Hyperoxia increases acid aspiration-induced inflammatory microvascular lung injury. This appears to be mediated by production of reactive species of O2.
authors.affiliation: Department of Anesthesiology, State University of New York, SUNY School of Medicine, Buffalo, USA. nnaderdj@ubmedb.buffalo.edu
authors.forename: N
authors.initials: N
authors.lastname: Nader-Djalal
authors.forename: P R
authors.initials: PR
authors.lastname: Knight
authors.forename: B A
authors.initials: BA
authors.lastname: Davidson
authors.forename: K
authors.initials: K
authors.lastname: Johnson
mesh_terms: D000818:Animals; D015824:Blood-Air Barrier / Q000502:physiology; D002196:Capillaries / Q000503:physiopathology; D005744:Gastric Acid; D006863:Hydrogen-Ion Concentration; D018496:Hyperoxia / Q000503:physiopathology*; D008168:Lung / Q000098:blood supply*; D008170:Lung Compliance; D008297:Male; D011015:Pneumonia, Aspiration / Q000209:etiology / Q000503:physiopathology*; D011446:Prospective Studies; D051381:Rats; D011919:Rats, Inbred Strains; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000503:physiopathology*; D013047:Specific Pathogen-Free Organisms; D013997:Time Factors