Tang G, Berg J T, White J E, Lumb P D, Lee C Y, Tsan M F
Research Service, Samuel S. Stratton Department of Veterans Affairs Medical Center, Albany, New York 12208.
Am J Physiol. 1994 Jan;266(1 Pt 1):L38-45. doi: 10.1152/ajplung.1994.266.1.L38.
Endotoxin and the cytokines, tumor necrosis factor and interleukin-1, are known to protect adult rats against O2 toxicity. However, whether the effect of endotoxin is mediated through its direct effect on lung cells or through cytokines is not clear. In this study, we demonstrated that endotoxin at a dosage of 5 micrograms/rat (14-20 micrograms/kg) attenuated O2-induced pulmonary injury and markedly prolonged the survival of rats exposed to 100% O2. Endotoxin was more protective when given by intratracheal insufflation or intravenous injection than by intraperitoneal injection. The endotoxin-induced O2 tolerance was associated with a selective enhancement of pulmonary manganese superoxide dismutase, but not Cu,Zn SOD, mRNA. In addition, depletion of 84% rat alveolar macrophages by liposome-encapsulated dichloromethylene diphosphonate, resulted in a marked reduction (86%) of endotoxin-induced release of tumor necrosis factor into the alveolar space. However, endotoxin was still protective in these alveolar macrophage-depleted animals.
内毒素以及细胞因子、肿瘤坏死因子和白细胞介素 -1 已知可保护成年大鼠免受氧中毒。然而，内毒素的作用是通过其对肺细胞的直接作用还是通过细胞因子介导尚不清楚。在本研究中，我们证明以 5 微克/大鼠（14 - 20 微克/千克）的剂量给予内毒素可减轻氧诱导的肺损伤，并显著延长暴露于 100%氧气的大鼠的存活时间。通过气管内注入或静脉注射给予内毒素比腹腔注射更具保护作用。内毒素诱导的氧耐受性与肺锰超氧化物歧化酶（而非铜锌超氧化物歧化酶）mRNA 的选择性增强有关。此外，用脂质体包裹的二氯亚甲基二膦酸盐使 84%的大鼠肺泡巨噬细胞耗竭，导致内毒素诱导的肿瘤坏死因子释放到肺泡腔中的量显著减少（86%）。然而，内毒素在这些肺泡巨噬细胞耗竭的动物中仍具有保护作用。
