【摘要】 目的　探讨实验性肺血栓栓塞症 (PTE)后血栓形成及其意义。方法　利用经热处理(70℃水浴 10min)的家兔自体血凝块 (0 0 4g/kg)制备急性PTE模型 ,通过肺脏解剖和病理研究PTE后血栓形成及其规律 ,并动态观察其凝血系统活性和血浆内皮素、血栓素A2 水平。结果　急性PTE后 1h有血栓形成倾向 ,2 4h有新鲜血栓形成 ,5d出现栓子全部或部分溶解 ,10、14d有血栓机化。栓塞后 2 4h凝血酶原时间 (7 15± 0 0 6 )s、纤维蛋白原 (5 86± 1 5 0 )g/L ,与栓塞前 (7 34± 0 19)s,(3 37± 1 0 2 )g/L比较差异有显著性 (P <0 0 5 )。静脉血浆血栓素A2 于栓塞后 5min [(2 5± 0 7)μg/L]开始升高 ,15min [(2 5± 0 6 ) μg/L]达峰值 ,与栓塞前 (0 6± 0 5 ) μg/L比较差异有显著性 (P <0 0 0 1) ,6 0min开始下降 (P >0 0 5 )。动、静脉血浆内皮素浓度均于栓塞后 5d [(0 84± 0 15 ) μg/L、(0 2 3± 0 0 5 ) μg/L]升高 ,与栓塞前 [(0 6 0± 0 45 ) μg/L、(0 15± 0 0 5 ) μg/L]比较差异有显著性 (P <0 0 5 )。结论　PTE后有血栓形成 ,栓塞后病理改变取决于血栓形成、溶解、机化三者间的相互作用 ,内皮素代谢障碍和血栓素A2 升高在发病中有重要作用更多还原

【Abstract】 Objective To study the significance of thrombosis after experimental pulmonary thromboembolism (PTE). Methods Acute PTE models of rabbits were established with injection of autologous blood clots (0.04 g/kg) stabilized in a temperature-controlled (70℃) of distilled water for 10 minutes through the femoral vein, then the regulation of thrombosis was explored at dissection and upon microscopic examination after PTE. Moreover, the coagulability of blood and the plasma level of thromboxane A 2 (TXA 2) and endothelin (ET) were examined. Results Thrombotic propensity was found at 1h, and fresh thrombosis started to form at 24 h following clots infusion. Emboli were completely or partly dissolved at 5 d and organized at 10 and 14 d after clots infused . Prothrombin time was significantly lower [(7.15±0.06)s],and fibrinogen was higher [(5.86±1.50) g/L] at 24 h post-clots, compared with pre-clots [(7.34±0.19)s, (3.37±1.02)g/L] (P<0.05). Venous plasma level of TXA 2 began to increase at 5 min [(2.5±0.7) μg/L] and continued to rise to its maximum at 15 min [(2.5±0.6) μg/L], then declined at 60 min after clots infusion. The level of ET in both arterial and venous blood increased at 5 d post-clots [(0.84±0.15)μg/L and (0.23±0.05)μg/L] separately, while most of emboli resolved. Conclusions There is thrombus formation after autologous-blood-clots-induced PTE. Furthermore, thrombus formation, fibrinolysis and organization may always interact on each other consistently, and control the pathogenesis of PTE. Abnormalities of ET metabolism occur after PTE and the major mediator of TXA 2 plays an important role in the early phase of PTE.更多还原