Jackson R M, Pisarello J B
Aviat Space Environ Med. 1984 Aug;55(8):709-14.
Rats pretreated with 500 micrograms X kg-1 endotoxin are resistant to the pulmonary toxic effects of normobaric hyperoxia (greater than 95% O2). After endotoxin-pretreatment and exposure to 1.0 ATA O2 for 72 h, such rats are found to have elevated total superoxide dismutase, glutathione peroxidase, and catalase activities in homogenates of whole lungs. Despite increases in these protective antioxidant enzymes which persist in 2.0 ATA O2 (4 h) and 4.0 ATA O2 (1.0 h), such rats do not have improved survival in hyperbaric hyperoxia. Likewise, endotoxin-pretreatment immediately prior to 2.0 or 4.0 ATA O2 exposure does not prolong survival compared to controls. It is likely that lung injury during the normobaric oxygen preexposure and the central nervous system toxicity of hyperbaric oxygen interact to limit survival.
用500微克/千克内毒素预处理的大鼠对常压高氧(大于95%氧气)的肺部毒性作用具有抗性。在内毒素预处理并暴露于1.0ATA氧气72小时后,发现此类大鼠全肺匀浆中的总超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶活性升高。尽管这些保护性抗氧化酶的活性增加,且在2.0ATA氧气(4小时)和4.0ATA氧气(1.0小时)环境中仍持续存在,但此类大鼠在高压高氧环境中的存活率并未提高。同样,与对照组相比,在暴露于2.0或4.0ATA氧气之前立即进行内毒素预处理并不能延长存活时间。常压氧气预暴露期间的肺损伤和高压氧的中枢神经系统毒性可能相互作用,从而限制了存活率。