Voss R, Matthias F R, Borkowski G, Reitz D
Department of Internal Medicine, Justus-Liebig-University, Giessen, F.R.G.
Br J Haematol. 1990 May;75(1):99-105. doi: 10.1111/j.1365-2141.1990.tb02623.x.
Disseminated thrombotic processes in the microcirculation are considered to be an important cause of multiple organ failure in septic patients. Fibrinolysis is one endogenous mechanism protecting the circulation from overwhelming thrombosis. Therefore, we looked for alterations of fibrinolytic parameters (tissue plasminogen activator (t-PA), tissue plasminogen activator inhibitor (PAI), D-dimer, euglobulin-clot-lysis-time (ECLT), plasminogen, alpha 2-antiplasmin) and of some coagulation parameters (prothrombin time, fibrinogen, platelets, antithrombin III, protein C, factor XII) in clearly defined septic patients and for the relations of these values to the severity of the disease (APACHE II-score). An increase in D-dimer and t-PA-antigen was registered in all patients, while factor XII and plasminogen were decreased, indicating an activated fibrinolysis. In contrast the systemic fibrinolytic capacity of the blood was strongly inhibited: t-PA-activity was not detectable, PAI-function was elevated, the ECLT was prolonged and alpha 2-antiplasmin was normal. Coagulation was moderately activated: the platelets, antithrombin III and protein C were decreased, the prothrombin time was prolonged and fibrinogen was normal. The changes in t-PA-antigen, PAI-function, factor XII, prothrombin time and antithrombin III were significantly related to the APACHE II-score of the patients. We conclude that the activation of coagulation is accompanied by an activation of fibrinolysis in the microcirculation, but that systemically the increased inhibitors of fibrinolysis (PAI, alpha 2-antiplasmin) induce a decrease of the fibrinolytic capacity of the blood. The severity of the disease determines the extent of the alterations.
微循环中的弥散性血栓形成过程被认为是脓毒症患者多器官功能衰竭的一个重要原因。纤维蛋白溶解是保护循环系统免受过度血栓形成影响的一种内源性机制。因此，我们研究了明确诊断的脓毒症患者纤维蛋白溶解参数（组织型纤溶酶原激活物（t-PA）、组织型纤溶酶原激活物抑制剂（PAI）、D-二聚体、优球蛋白凝块溶解时间（ECLT）、纤溶酶原、α2-抗纤溶酶）以及一些凝血参数（凝血酶原时间、纤维蛋白原、血小板、抗凝血酶III、蛋白C、因子XII）的变化，以及这些值与疾病严重程度（急性生理与慢性健康状况评分系统II（APACHE II）评分）之间的关系。所有患者的D-二聚体和t-PA抗原均升高，但因子XII和纤溶酶原降低，表明纤维蛋白溶解被激活。相反，血液的全身纤维蛋白溶解能力受到强烈抑制：未检测到t-PA活性，PAI功能升高，ECLT延长，α2-抗纤溶酶正常。凝血呈中度激活：血小板、抗凝血酶III和蛋白C降低，凝血酶原时间延长，纤维蛋白原正常。t-PA抗原、PAI功能、因子XII、凝血酶原时间和抗凝血酶III的变化与患者的APACHE II评分显著相关。我们得出结论，凝血激活伴有微循环中纤维蛋白溶解的激活，但在全身，纤维蛋白溶解抑制剂（PAI、α2-抗纤溶酶）增加导致血液纤维蛋白溶解能力下降。疾病的严重程度决定了变化的程度。
