摘要
目的:用内毒素(ET)静注复制家兔急性肺损伤(ALI)模型,测定模型不同时间点微血管内皮细胞释放血管性假血友病因子(vWF)的变化,并用氯喹干预,以揭示微血管内皮细胞在ALI中的受损机制,并寻找有效的干预药物。方法:设A组(对照组)、B组(损伤组)和C组(损伤+干预组),A组静注生理盐水对照,B组按600μg/kg剂量静脉注射ET,复制家兔ALI模型,C组同等剂量静注ET后,按5 mg/kg剂量静注氯喹,分别测量用药前和用药后0.5 h、1 h、2 h、4 h动脉血的氧分压、血清中丙二醛(MDA)、超氧化物歧化酶(SOD)及血浆中vWF含量,比较三组之间的差别。结果:B组vWF活性和MDA含量明显高于A组,而SOD降低;C组也有类似变化,但变化幅度较B组小,三组之间比较相差显著。结论:血浆中vWF活性增高,是ALI的重要标志;应用氯喹后血浆中vWF活性明显降低,证实其对肺微血管内皮细胞具有一定的保护作用。
Objective： To study the changes of yon Willebrand Factor（vWF） come from endothelial in blood plasma in endotoxin（ ET）-induced acute lung injury（ALl） in rabbits, to observe the interference effects of chloroquine on vWF to reveal the principle of endothelial cell damage in ALl, and to find out effective therapeutic method for ALl in clinic. Methods： 24 rab- bits were randomly assigned to three groups： group A（ control group）, group B（ ET group）, and group C（ ET and chloroquine group）. ALl was induced by intravascular injection of ET（600 ~g/kg）. The rabbits of group C were injected by chloroquine af- ter ET injection. The vWF. malondialdehyde（MDA） .superoxide dismutase（SOD） and Pa02 were measured before injection and 0.5 h, 1 h, 2 h, 4 h after injection in every group. The results were analyzed. Results： VWF and MDA were higher in group B than that in group A. But SOD in group B was lower than that in group A. The results of group C were similar with group B but the extents of changes were lower than that in group B. The differences of every group were significant. Conclusion： The change of vWF is one of the identifications in ALl. Chloroquine injection can depress the action of vWF. So chlorquine has protective effect to endothelial cell in ALl.
出处
《军医进修学院学报》
CAS
北大核心
2008年第4期300-302,共3页
Academic Journal of Pla Postgraduate Medical School
