Carvalho A C, DeMarinis S, Scott C F, Silver L D, Schmaier A H, Colman R W
Section of Hematology, Veterans Administration Medical Center, Providence, Rhode Island.
J Lab Clin Med. 1988 Aug;112(2):270-7.
Adult respiratory distress syndrome (ARDS) is a complex pulmonary clinicopathologic condition associated with pulmonary endothelial injury and blood coagulation activation. In patients with ARDS from all causes, factor VII levels were significantly reduced. Patients with ARDS caused by sepsis had more evidence of intravascular coagulation and fibrinolysis than did patients with trauma-related ARDS by having significantly (p less than or equal to 0.05) increased prothrombin times, activated partial thromboplastin times, and fibrin degradation products, and decreased antithrombin III concentration. We sought to determine whether the proteins of the contact system of plasma proteolysis (factor XII, prekallikrein, high molecular weight kininogen, and C1 inhibitor) were also activated after acute lung injury. Patients with ARDS caused by either trauma or sepsis had significantly (p less than or equal to 0.01) reduced factor XII levels, high molecular weight kininogen functional activity, prekallikrein activity, and prekallikrein antigen levels compared with controls. In both the sepsis-related and trauma-related ARDS groups, C1 inhibitor activity was significantly reduced but C1 inhibitor antigen levels were significantly elevated from control. These findings showed that the proteins of the contact system were more extensively activated in ARDS than were the proteins that contribute to later reactions in intravascular coagulation and fibrinolysis. Activation of the contact system proteins could be the result of endothelial injury occurring as part of ARDS. Intravascular coagulation and fibrinolysis in patients with ARDS also arise from components independent from contact system activation.
成人呼吸窘迫综合征（ARDS）是一种与肺内皮损伤和凝血激活相关的复杂的肺部临床病理状况。在所有病因导致的ARDS患者中，凝血因子VII水平显著降低。脓毒症所致ARDS患者比创伤相关ARDS患者有更多血管内凝血和纤维蛋白溶解的证据，前者的凝血酶原时间、活化部分凝血活酶时间和纤维蛋白降解产物显著升高（p≤0.05），抗凝血酶III浓度降低。我们试图确定血浆蛋白水解接触系统的蛋白质（因子XII、前激肽释放酶、高分子量激肽原和C1抑制剂）在急性肺损伤后是否也被激活。与对照组相比，创伤或脓毒症所致ARDS患者的因子XII水平、高分子量激肽原功能活性、前激肽释放酶活性和前激肽释放酶抗原水平显著降低（p≤0.01）。在脓毒症相关和创伤相关ARDS组中，C1抑制剂活性显著降低，但C1抑制剂抗原水平比对照组显著升高。这些发现表明，与促成血管内凝血和纤维蛋白溶解后期反应的蛋白质相比，接触系统的蛋白质在ARDS中被更广泛地激活。接触系统蛋白质的激活可能是ARDS所致内皮损伤的结果。ARDS患者的血管内凝血和纤维蛋白溶解也源于独立于接触系统激活的成分。
