Witte J, Jochum M, Scherer R, Schramm W, Hochstrasser K, Fritz H
Intensive Care Med. 1982;8(5):215-22. doi: 10.1007/BF01694524.
This study was performed on patients (n = 18) suffering from strictly defined hyperdynamic septic shock. Plasma factors (C-reactive protein, acid alpha 1-glycoprotein, fibrinogen, fibrinopeptide A, fibrinogen-fibrin split products, factor XIII, antithrombin III, complement factors C3 and C4, inter-alpha-trypsin-inhibitor and alpha 2-macroglobulin) measured during hyperdynamic septic shock were highly abnormal. The activation and consumption of clotting, fibrinolytic and complement factors due to system-specific proteinases (such as thrombokinase or plasminogen activators) seemed to be intensified by the nonspecific proteolytic activity of granulocytic proteinases probably released by the action of endotoxins. Possible therapeutic measures to maintain the endogeneous defence mechanism against enhanced proteolysis during septic shock are discussed.
本研究针对患有严格定义的高动力性感染性休克的患者(n = 18)进行。在高动力性感染性休克期间测量的血浆因子(C反应蛋白、酸性α1-糖蛋白、纤维蛋白原、纤维蛋白肽A、纤维蛋白原-纤维蛋白裂解产物、因子XIII、抗凝血酶III、补体因子C3和C4、α-胰蛋白酶抑制剂和α2-巨球蛋白)高度异常。由于系统特异性蛋白酶(如凝血激酶或纤溶酶原激活剂)导致的凝血、纤维蛋白溶解和补体因子的激活及消耗,似乎因内毒素作用可能释放的粒细胞蛋白酶的非特异性蛋白水解活性而加剧。文中讨论了在感染性休克期间维持针对增强的蛋白水解的内源性防御机制的可能治疗措施。