Hyperoxia exacerbates microvascular lung injury following acid aspiration.
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.
Nader-Djalal
N
N
Department of Anesthesiology, State University of New York, SUNY School of Medicine, Buffalo, USA. nnaderdj@ubmedb.buffalo.edu
Knight
P R
PR
Davidson
B A
BA
Johnson
K
K
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