血管内皮细胞损伤在肾综合征出血热出血机制中的作用

Study on the effects of vascular endotheliocyte damage on the pathogenesis of hemorrhage fever with renal syndrome

目的 探讨肾综合征出血热 (HFRS)时血管内皮细胞的功能变化。方法 用出血时间测定器、酶联免疫吸附、放射免疫分析、发色底物及胶乳凝集试验检测出血时间 (BT)、血管性血友病因子抗原 (vWF :Ag)、6 酮PGF1α(6 Keto)、组织纤溶酶原激活物活性 (t PA)、纤溶酶原激活抑制物 1活性 (PAI 1:A)、内皮素 1(ET 1)、血纤维蛋白 (原 )降解产物 (FDP)。结果 除轻型患者的t PA :A、PAI 1:A、ET 1外 ,其他各型患者所测的指标与正常对照组相比差异均有显著性 (P <0 .0 5 ,P <0 .0 0 1)。各指标的动态观察发现除个别轻型患者外 ,vWF :Ag、ET 1、t PA及FDP的血浆水平均随病程的进展而升高 ,6 酮 PGF1α在发病初期即有显著下降 ,休克期达最低 ,并随病情的缓解而趋向正常。结论 在肾综合征出血热时 。

Objective To study the functional change of vascular endotheliocytes in hemorrhage fever with renal syndrome (HFRS). Methods The bleeding time (BT), von Willebrand Factor antigen (vWF:Ag), 6 keto PGF 1α(6 Keto), tissue type plasminogen activator (t PA), plasminogen activator inhibitor 1 activity (PAI 1: A), endothelin 1 (ET 1) and fibrin degradation product (FDP) were measured using template method, ELISA, radioimmunology analysis, color substrate and latex aggregating test. Results All the above parameters varied significantly comparing the normal controls ( P <0.05～0.001) except for t PA:A, PAI 1:A and ET 1 in mild patients. vWF:Ag, ET 1, t PA:A and FDP were progressively increasing as the disease proceeded except for some mild patients. 6 Keto decreased significantly in the early stage, reached bottom in the shock stage and gradually returned to normal when the patients recovered. Conclusions Damages in vascular endotheliocytes of various extents exist in HFRS patients.