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Abstract
The role of endogenous tumor necrosis factor (TNF) in the pathogenesis of pulmonary O2 toxicity was investigated. Intratracheal insufflation of anti-TNF antibodies prolonged the survival of rats exposed to 100% O2. No TNF bioactivity or immunoreactive protein was detectable in the alveolar lavage fluid or lung homogenate of rats exposed to normoxia or hyperoxia. However, levels of pulmonary TNF mRNA were markedly enhanced in rats exposed to hyperoxia. These results suggest that hyperoxia may cause the production of low level TNF, which in turn enhances O2 toxicity.
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