大鼠出血性休克后肠源性内毒素血症及TNF、IL-1变化的动态观察

Experimental study on gut-derived endotoxemia and the changes of TNF, IL-1 levels following hemorrhagic shock in rats

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。

The purpose of this study was to observe dynamically the changes oftumor necrosis factor (TNF), interleukin l (IL-1) levels, and the relationship betweenthe changes and gut-derived endotoxemia following hemorrhagic shock (4.00 kPa for 90minutes). The results showed that the content of endotoxin in both portal and systemicblood was markedly increased (P<0.05～0.01) after injury. Endotoxin content of portalvein paralleled with the change of TNF in systemic plasma, but its peak TNF level occu-rred much earlier than that occurred in systemic plasma. Marked elevation of IL-1 activityof peritoneal macrophages was not seen until 6 hours following resuscitation, and wassustained up to 24 hours. Pretreatment with polymyxin B could attenuate the increaseof endotoxin content significantly in both portal and systemic blood, and also inhibitedthe production and release of TNF, IL-1 in the body at this time. The survival rate in thetreated group increased 33.4% as compated with control group. The results indicated thatgut-derived endotoxemia appeared quite early, and had marked influence on the changesof TNF IL-1 levels following hemorrhagic shock. It was therefore postulated thatboth these cytotoxines which well produced and released in excess might have pathogenicroles in sevre injury of the host.