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目的了解急性肺栓塞(PTE)患者发病后及抗凝或溶栓治疗后凝血纤溶系统和血管内皮功能的变化。方法将37例 PTE 患者分为抗凝治疗组(20例)和溶栓治疗组(17例),设立正常对照组40例,采用 ELISA 法检测血浆D-二聚体(D-D)、组织型纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制剂-1(PAI-1)、蛋白-S(PS)、蛋白-C(PC)、凝血酶调节货白(TM)含量,采用发色底物法检测抗凝血酶-Ⅲ(AT-Ⅲ)活性。在抗凝治疗第6天和溶栓结束后24 h 分别复查上述指标。抗凝治疗患者可应用静脉注射普通肝素或采用皮下注射低分子肝素。在应用普通肝素或低分子肝素24～48 h后,加用口服抗凝剂华法林,重叠应用4～5 d,当连续2 d 测定凝血酶原时间(PT)国际标准比值(TNR)达到2.0～3.0时,停用普通肝素/低分子肝素,单独口服华法林治疗。溶栓治疗组患者采用尿激酶或 rtPA 溶栓。在应用低分子肝素24～48 h 后加用口服抗凝剂华法林,重叠应用4～5 d,当连续2 d 测定 PT INR 达到2.0～3.0时,停用低分子肝素,单独口服华法林治疗。结果在治疗前,抗凝治疗组 PTE 患者 D-D、t-PA、PS、TM 含量明显高于正常对照组,AT-Ⅲ活性明显低于正常对照组(均 P<0.05);溶栓治疗组 PTE 患者 D-D、t-PA、PAI-1、PS、TM 含量明显高于正常对照组,AT-Ⅲ活性明显低于正常对照组(均 P<0.05)。抗凝治疗组应用肝素或低分子肝素后血 D-D、t-PA、PS、PC 含量较治疗前有明显下降(均 P<0.05),而 PAI-1、TM 含量和 AT-Ⅲ活性治疗前后差异无统计学意义。溶栓治疗组应用尿激酶或 rtPA 溶栓后,血 D-D、t-PA、PAI-1、PS、PC、TM 含量较治疗前有明显下降(均 P<0.05),而 AT-Ⅲ活性较治疗前差异无统计学意义。结论 PTE 患者存在凝血纤溶系统功能失衡和肺血管内皮损伤。抗凝和溶栓治疗对于调节 PTE 患者体内的凝血与纤溶系统失衡及血管内皮功能有重要意义。
Objective To investigate the changes of coagulation and fibrinolytic system and endothelial function after acute pulmonary embolism (PTE) onset and after anticoagulation or thrombolysis. Methods Thirty-seven patients with PTE were divided into anticoagulation group (n = 20) and thrombolytic group (n = 17). Forty normal controls were enrolled in this study. The levels of plasma D-dimer (T-PA), plasminogen activator inhibitor-1 (PAI-1), protein S (PS), protein C (PC) , Using chromogenic substrate method for detecting antithrombin-Ⅲ (AT-Ⅲ) activity. The above indexes were respectively reviewed on the 6th day of anticoagulant therapy and 24 hours after the end of thrombolysis. Patients with anticoagulant therapy can be given intravenous unfractionated heparin or subcutaneous injection of low molecular weight heparin. After application of unfractionated heparin or low molecular weight heparin for 24-48 h, oral anticoagulant warfarin was added for 4 to 5 days. When the international standard ratio (PT) of prothrombin time (PT) reached 2.0 ~ 3.0, disable the unfractionated heparin / low molecular weight heparin, oral warfarin alone. Patients in the thrombolytic group received urokinase or rtPA thrombolysis. Low-molecular-weight heparin was added to oral anticoagulant warfarin 24 to 48 hours after application for 4 to 5 days. When the PT INR reached 2.0 to 3.0 for 2 days, low-molecular-weight heparin Lin treatment. Results Before treatment, the levels of DD, t-PA, PS and TM in patients with PTE in anticoagulant therapy group were significantly higher than those in normal control group, and AT-Ⅲ activity was significantly lower in patients with PTE than in normal control group (all P <0.05) The levels of DD, t-PA, PAI-1, PS and TM in patients were significantly higher than those in normal controls (P <0.05). The levels of DD, t-PA, PS and PC in the blood of anticoagulant therapy group were significantly lower than those before treatment (P <0.05), while the levels of PAI-1, TM and AT- No statistical significance. The levels of DD, t-PA, PAI-1, PS, PC and TM in thrombolytic therapy group decreased significantly (all P <0.05), while the activity of AT- Before the difference was not statistically significant. Conclusion The coagulation and fibrinolysis system in PTE patients have imbalanced function and pulmonary vascular endothelial injury. Anticoagulation and thrombolytic therapy for the regulation of PTE in patients with coagulation and fibrinolytic system imbalance and endothelial function is important.