中文摘要：

目的比较以纤维化为主的特发性肺纤维化（IPF）和以炎症表现为主的非特发性肺纤维化的特发性间质性肺炎（nIPF_IIP）患者的支气管肺泡灌洗液（BAI，F）和血浆中尿激酶型纤溶酶原激活物（u-PA）、组织型纤维蛋白酶原激活物（t-PA）、纤溶酶原激活物抑制物-1（PAI-1）的差异，探讨纤溶活性异常与特发性间质性肺炎（IIP）类型或纤维化程度的关系。方法研究对象包括IIP患者144例，其中IPF患者102例（IPF组），nIPF-IIP患者42例（nIPFdIP组）；对照组26名。采用ELISA测定BALF和血浆中u-PA、t-PA和PAI-1含量。结果①IPF和nIPF-IIP患者BALF中u-PA分别为（O．20±0．01）／ug／L和（O．22±0．01）／ug／L，与对照组[（O．27土0．01）tug／L]比较明显降低，差异均有统计学意义（P〈O．01）。②IPF和nIPF-IIP患者血浆t_PA较对照组明显升高（P〈0．01）。③IPF和nIPF-IIP患者BALF中PAI-1分别为（4．054-0．85）／ug／L和（3．69±0．88）／ug／L，高于对照组[（1．11±0．12）Fg／L，P〈O．05或P〈O．01]；血浆中PAI-1在各型IIP患者也明显升高，差异有显著统计学意义（P〈O．01）。结论无论是以纤维化表现为主的IPF，还是以炎症表现为主的nIPF-IIP，肺脏都表现以u-PA降低和PAI-1增加为特征的纤溶活性降低和纤溶抑制活性增强；循环中主要表现以PAI-1增加为特征的纤溶抑制水平增加。这种纤溶活性降低似乎在IPF表现更明显。关于以u-PA和PAI-1为代表的纤溶系统在肺纤维化的作用机制及其与IIP类型或纤维化程度的确切关系值得进一步研究。

英文摘要：

Objective To detect and compare the levels of urokinase plasminogen activator （u-PA）, tissue plasminogen activator （t-PA）, and plasminogen activator inhibitor-1 （PAI 1） in the bronchoalveolar lavage fluid （BALF） and the plasma of patients with idiopathic interstitial pneumonia （IIP） with predominant fibrosis or inflammation. Methods BALF and plasma were derived from 144 patients with IIP including 102 cases of idiopathic pulmonary fibrosis （IPF） and 42 non-IPF cases of IIP （nIPF-IIP）, and 26 controls. Results u-PA levels in BALF of patients with IPF [（0.20-4-0.01） tug/L] and nlPF-IIP [-（0.22-4-0.01） /ug/L] were significantly decreased compared with controls [（0.27 ± 0.01） rig/L, P 〈0.01]. PAId levels in BALF of patients with IPF [（4.05±0.85） gg/L] and nIPF-IIP [（3.69±0.88） tug/L] were significantly increased compared with controls [（1.11±0.12） rig/L, P 〈 0.05 or P 〈0.01. Both t-PA and PAI-1 levels in plasma were significantly elevated in patients with IIP （P 〈0.01）. Conclusions There is depressed fibrinolytic or enhanced anti-fibronolytic activity in the lung of patients with IPF and nIPF-IIP, characterized by decreased u-PA and increased PAId. There is augmented anti-fibronolytic activity in plasma presented with elevated PAI-1 in patients with IPF and nIPF-IIP. Such decrease fibrinolysis in patients with IPF and nIPF-IIP, especially in IPF, maybe promote the development of pulmonary fibrosis. It is warranted to study the role of fibronolytic system composedmainly of u-PA and PAI-1 in pathogenesis of pulmonary fibrosis, correlation with the subtype of IIP or the degree of fibrosis.