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实验性肺血栓栓塞症后血栓形成及其意义
引用本文:季颖群,关宏伟,谷玲,李敬,张延军,张学武,徐岳红,谭园园,张中和. 实验性肺血栓栓塞症后血栓形成及其意义[J]. 中华结核和呼吸杂志, 2001, 24(12): 718-721
作者姓名:季颖群  关宏伟  谷玲  李敬  张延军  张学武  徐岳红  谭园园  张中和
作者单位:1. 大连医科大学附属第一医院呼吸内科,
2. 大连医科大学附属第一医院病理科,
3. 大连医科大学附属第一医院核医学,
4. 大连医科大学附属第一医院检验科
基金项目:国家"九五"科技重点攻关资助项目(96-907-01-04)
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10 min)的家兔自体血凝块(0.04 g/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1 h有血栓形成倾向,24 h有新鲜血栓形成,5 d出现栓子全部或部分溶解,10、14 d有血栓机化.栓塞后24 h凝血酶原时间(7.15±0.06) s、纤维蛋白原(5.86±1.50) g/L,与栓塞前(7.34±0.19) s,(3.37±1.02) g/L比较差异有显著性(P<0.05).静脉血浆血栓素A2于栓塞后5 min [(2.5±0.7)μg/L]开始升高,15 min [(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<0.001),60 min开始下降(P>0.05).动、静脉血浆内皮素浓度均于栓塞后5 d [(0.84±0.15)μg/L、(0.23±0.05) μg/L]升高, 与栓塞前[(0.60±0.45) μg/L、(0.15±0.05) μg/L]比较差异有显著性(P<0.05). 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.

关 键 词:血栓形成 血栓素A2 内皮素 肺血栓栓塞症 实验研究
修稿时间:2001-07-10

The significance of thrombosis after experimental pulmonary thromboembolism
JI Yingqun,GUAN Hongwei,GU Ling,et al.. The significance of thrombosis after experimental pulmonary thromboembolism[J]. Chinese journal of tuberculosis and respiratory diseases, 2001, 24(12): 718-721
Authors:JI Yingqun  GUAN Hongwei  GU Ling  et al.
Affiliation:First Affiliated Hospital of Dalian Medical University, Dalian 116011, China.
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 degrees C) 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 A2(TXA2) and endothelin (ET) were examined. RESULTS: Thrombotic propensity was found at 1 h, 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 TXA2 began to increase at 5 min [(2.5 +/- 0.7) micrograms/L] and continued to rise to its maximum at 15 min [(2.5 +/- 0.6) micrograms/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) micrograms/L and (0.23 +/- 0.05) micrograms/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 TXA2 plays an important role in the early phase of PTE.
Keywords:Thrombosis  Thromboxane A 2  Endothelin  Pulmonary thromboembolism
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