Agrenius V, Chmielewska J, Widström O, Blombäck M
Department of Clinical Chemistry, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
Am Rev Respir Dis. 1989 Nov;140(5):1381-5. doi: 10.1164/ajrccm/140.5.1381.
Chronic malignant pleural exudation is generally characterized by little or no fibrin deposition. However, during induced inflammation, fibrin deposition concomitant with cessation of exudation is seen. To judge the involvement of the fibrinolytic system in this process, concentrations of fibrinolytic factors were followed in 10 patients during treatment by quinacrine instillation and tube drainage. Plasminogen and alpha-2-antiplasmin were found in low concentrations and did not show significant changes during treatment. The plasminogen activator inhibitor PAI-1, which plays an important role in the regulation of fibrinolysis, was also studied during treatment. Before treatment the concentration of PAI-1 was 21.7 +/- 12.0 (mean +/- SD) AU/ml and it increased to 86.9 +/- 25.9 AU/ml 6 h after quinacrine instillation. D-dimer, a product of the lysis of fibrin, was found in high concentrations before treatment (62.7 +/- 25.5 micrograms/ml) and in low concentrations 6 h after treatment (12.2 +/- 7.9 micrograms/ml). Thus, it was possible to demonstrate that the fibrinolytic system is activated during chronic malignant pleural exudation and, furthermore, that the activity decreases during induced inflammation.
慢性恶性胸腔积液通常的特征是几乎没有或仅有少量纤维蛋白沉积。然而，在诱导炎症期间，可观察到纤维蛋白沉积伴随着渗出停止。为了判断纤溶系统在这一过程中的作用，在10例接受喹吖因灌注和胸腔闭式引流治疗的患者中监测了纤溶因子的浓度。发现纤溶酶原和α2抗纤溶酶浓度较低，且在治疗期间未显示出显著变化。在治疗期间还研究了在纤溶调节中起重要作用的纤溶酶原激活物抑制剂PAI-1。治疗前PAI-1浓度为21.7±12.0（均值±标准差）AU/ml，喹吖因灌注后6小时升至86.9±25.9 AU/ml。纤维蛋白溶解产物D-二聚体在治疗前浓度较高（62.7±25.5微克/毫升），治疗后6小时浓度较低（12.2±7.9微克/毫升）。因此，有可能证明在慢性恶性胸腔积液期间纤溶系统被激活，而且在诱导炎症期间其活性降低。
