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本实验采用大鼠出血性休克模型(4.00kPa,90min)动态观察了TNF、IL-1等细胞因子的变化规律及其与肠源性内毒素血症的关系。研究发现:休克组动物休克后门、体循环均出现显著的内毒素血症,门脉系统血浆内毒素水平的变化趋势与外周血TNF一致,但其峰值早于后者。同时,腹腔巨噬细胞IL-1活性在复苏后6～24h亦持续升高。休克治疗组给予多粘菌素B预防性治疗后,动物门、体循环内毒素含量均迅速下降,TNF、IL-1的产生显著抑制,动物存活率比休克组提高33.4%。结果提示,休克后早发的肠源性内毒素血症对宿主单核巨噬细胞诱生TNF、IL-1有明显影响。出血性休克初期TNF、IL-1等细胞因子的过度产生、释放可能参与了机体的免疫损伤过程。
In this study, the hemorrhagic shock model of rats (4.00kPa, 90min) dynamically observed the changes of TNF, IL-1 and other cytokines and its relationship with intestinal endotoxemia. The study found that: shock shock shock in the back door, the systemic circulation were significant endotoxemia, plasma endotoxin levels in portal system trends and peripheral blood TNF consistent, but the peak earlier than the latter. At the same time, IL-1 activity of peritoneal macrophages also continued to increase 6 ~ 24h after resuscitation. After the preventive treatment of polymyxin B in shock treatment group, the levels of endotoxin in the gonads and systemic circulation decreased rapidly, and the production of TNF and IL-1 was significantly inhibited. The survival rate of animals was increased by 33.4% compared with that of shock group. The results suggest that early onset of shock after endotoxemia of host induced monocyte-macrophage TNF, IL-1 have a significant impact. Hemorrhagic shock initial TNF, IL-1 and other cytokines over-production, release may be involved in the body’s immune injury process.