Redl H, Nikolai A, Kneidinger R, Schlag G
Ludwig-Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria.
Behring Inst Mitt. 1993 Aug(92):218-28.
Vascular endothelial-PMN interactions are critical reactions in the development of organ failure. Both cell types are activated by LPS and proinflammatory cytokines in sepsis. Reactions that are collectively referred to as endothelial activation include expression of procoagulant activity and increased adhesiveness of the endothelium for leukocytes. Some parameters, which are related to endothelial activation are significantly changed during sepsis and altered by anti-TNF therapy (e.g. PAI-1, thrombomodulin), while others (e.g. sELAM) are increased by sepsis but not influenced by anti-TNF therapy. Leukocyte activation (accompanied by elastase release) leads to rearrangement of the CD11/CD18 structures and thereby increased adherence.
血管内皮细胞与中性粒细胞的相互作用是器官衰竭发展过程中的关键反应。在脓毒症中，这两种细胞类型均会被脂多糖和促炎细胞因子激活。统称为内皮细胞激活的反应包括促凝活性的表达以及内皮细胞对白细胞黏附性的增加。一些与内皮细胞激活相关的参数在脓毒症期间会发生显著变化，并可通过抗TNF治疗而改变（如纤溶酶原激活物抑制剂-1、血栓调节蛋白），而其他参数（如可溶性内皮白细胞黏附分子）则会因脓毒症而升高，但不受抗TNF治疗的影响。白细胞激活（伴随着弹性蛋白酶释放）会导致CD11/CD18结构重排，从而增加黏附性。
