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细菌性脓毒症及其最严重的并发症脓毒性休克在获得性凝血紊乱的发病机理中起十分重要的作用。革兰氏阴性细菌的细胞壁释放的内毒素先损害内皮细胞,继而激活凝血、纤维蛋白溶解和补体系统;内毒素和炎性介质可直接引起白细胞脱颗粒,释放出溶酶体酶,其中蛋白酶如凝血激酶和纤维蛋白溶酶原激活质可特异性地激活凝血、纤维蛋白溶解和补体三个系统,导致弥漫性血管内凝血,而内毒素使白细胞释放的蛋白酶如弹性硬蛋白酶和组织蛋白酶G却非特异性地消耗血浆蛋白因子。其结果是血浆蛋白的严重紊乱。本文在严格定义的脓毒性休克病人中测定某些血浆因子的变化,以研究特异性激活和非特异性蛋白分解的降解作用在消耗血浆蛋白因子中的作用。
Bacterial sepsis and its most serious complication Septic shock plays a very important role in the pathogenesis of acquired coagulopathy. Endotoxin released from the cell walls of Gram-negative bacteria preferentially damages endothelial cells, which in turn activates coagulation, fibrinolysis and the complement system; endotoxins and inflammatory mediators can directly cause leukocyte degranulation and release of lysosomal enzymes such as proteases Thromboplastin and plasminogen activators specifically activate the three systems of coagulation, fibrinolysis and complement, resulting in disseminated intravascular coagulation, whereas endotoxin releases leukocytes such as elastase and cathepsin G Non-specific depletion of plasma protein factor. The result is a serious disorder of plasma proteins. We herein assayed for changes in certain plasma factors in strictly defined septic shock patients to investigate the role of specific activation and degradation of nonspecific proteolysis in the depletion of plasma protein factors.