摘要
首先用全血内毒素血症动物模型，以内毒素刺激全血，显示动物上清液肿瘤坏死因子（ＴＮＦα）浓度随内毒素剂量增加而增加，地塞米松明显抑制其释放，布洛芬对αＴＮＦα释放为双向效应。腹腔注射内毒素复制大鼠急性肺损伤模型，显示肺毛细血管通透性随内毒素剂量增大而增加，提前１小时注射地塞米松、布洛芬能防止血管通透性增加；同时观察到肺组织中ＴＮＦα、白细胞介素１β（ＩＬ１β）、巨噬细胞炎性蛋白１α（ＭＩＰ１α）及ｍＲＮＡ含量随内毒素剂量增大而增多，峰值在２，６和１２小时，地塞米松、布洛芬对肺组织中细胞因子表达具有明显抑制。说明ＴＮＦα、ＩＬ１β、ＭＩＰ１α在内毒素诱发的肺损伤中起重要作用，地塞米松、布洛芬通过抑制细胞因子表达。
We used the animal model of endotoxemia (endotoxin was used to stimulate the whole blood) The result showed that the concentration of the supernatant blood tumor necrosis factor (TNFα) increased with increasing doses of endotoxins Dexamethasone obviously inhibited the release of TNFα,while ibuprofen had dual efects on TNFα In acute lung injury in rats induced by penitoncal injection of endotoxins, the permeability of the pulmonary capillaries increased with increasing doses of endotoxins. Injection of dexamethasone and ibuprofen 1hr ahead of time could prevent the increase of the vascular permeability Meanwhile,the pulmonary contents of TNFα,interleukin1β(IL1β),macrophage inflammation protein1α(MIP1α) and mRNA increased with increasing doses of endotoxins,their peak values being at 2,6,and 12hr respectively. Dexamethasone and ibuprofen markedly inhibited the expression of the cellular factor in the pulmonary tissues It is suggested that TNFα,IL1β and MIP1α play an important role in pulmonary injury induced by endotoxins,and dexamethasone and ibuprofen can protect the acutely injured lungs by inhibiting the eapression of the cellular factor.
出处
《中国危重病急救医学》
CSCD
1996年第3期139-142,共4页
Chinese Critical Care Medicine
关键词
肿瘤坏死因子
IL-Β
感染
内毒素
治疗
tumor necrosis factor
interleukin1β
macrophage inflammation protein1α
infection
endotoxin
treatment
