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Articles in PresS, published online ahead of print April 15, 2002
J Appl Physiol, 10.1152/jap.00570.2001
Submitted on June 4, 2001
Accepted on April 8, 2002
1 Pulmonary/Critical Care Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: dquinn1{at}partners.org.
The use of positive pressure mechanical ventilation can cause ventilator-induced lung injury (VILI). We hypothesized that hyperoxia in combination with large tidal volumes (VT) would accentuate non-cardiogenic edema and neutrophil infiltration in VILI and be dependent on stretch-induced MIP-2 production. In rats ventilated with VT 20 cc/kg, there was pulmonary edema formation which was significantly increased by hyperoxia. Total lung neutrophil infiltration, and MIP-2 in bronchoalveolar lavage (BAL) fluid were significantly elevated both in animals exposed to high VT on room air (RA) and with hyperoxia. Hyperoxia markedly augmented the migration of neutrophils into the alveoli. Anti-MIP-2 antibody blocked migration of neutrophils into the alveoli in RA by 51% and with hyperoxia by 65%. We concluded that neutrophil migration into the alveoli was dependent on stretch-induced MIP-2 production. Hyperoxia significantly increased edema formation and neutrophil migration into the alveoli with VT 20 cc/kg, although BAL MIP-2 levels were nearly identical to VT 20 cc/kg with RA, suggesting other mechanisms may be involved in hyperoxia augmented neutrophil alveolar content in VILI.
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