Tsan M F, White J E, Michelsen P B, Wong G H
Samuel S. Stratton Department of Veterans Affairs Medical Center, Albany, New York, USA.
Exp Lung Res. 1995 Jul-Aug;21(4):589-97. doi: 10.3109/01902149509031761.
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.
研究了内源性肿瘤坏死因子（TNF）在肺部氧中毒发病机制中的作用。气管内注入抗TNF抗体可延长暴露于100%氧气环境下大鼠的存活时间。在暴露于常氧或高氧环境下的大鼠肺泡灌洗液或肺匀浆中，未检测到TNF生物活性或免疫反应性蛋白。然而，暴露于高氧环境下的大鼠肺组织TNF mRNA水平显著升高。这些结果表明，高氧可能导致低水平TNF的产生，进而增强氧毒性。
