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急性脑梗死发作期间组织因子途径改变的观察
引用本文:文志斌,熊石龙,何晓凡,何美霞,贺石林,解勤之,蹇在伏,陈方平,肖波,杨期东. 急性脑梗死发作期间组织因子途径改变的观察[J]. 中国危重病急救医学, 2003, 15(9): 529-531
作者姓名:文志斌  熊石龙  何晓凡  何美霞  贺石林  解勤之  蹇在伏  陈方平  肖波  杨期东
作者单位:1. 中南大学湘雅医学院生理学系止血与血栓研究室,湖南,长沙,410078
2. 中南大学湘雅医院,湖南,长沙,410008
基金项目:国家自然科学基金重点资助项目(39830 180 )
摘    要:目的 :观察急性脑梗死 (ACI)与组织因子途径变化以及与该途径有关的其他凝血因子的关系。方法 :71例经 CT确诊为 ACI患者和 5 0名正常人被纳入研究范围。血浆中组织因子 (TF)和组织因子途径抑制物(TFPI)活性测定采用发色底物法 ;抗原测定用酶联免疫吸附法 (ELISA) ;血浆中 F 促凝活性 (F ∶C)和F 促凝活性 (F ∶C)测定用一期凝固法 ;凝血酶原 (F )的活性测定采用 Ecarin法 ;纤维蛋白原 (Fbg)的活性测定采用凝血酶法 ;抗凝血酶 (AT )的测定用肝素辅因子法。结果 :与正常对照组比较 ,ACI患者血浆中TF活性显著增加 (P<0 .0 5 ) ,TF抗原含量显著增加 (P<0 .0 5 ) ,TFPI的活性降低 (P<0 .0 5 ) ,TFPI抗原含量明显降低 (P<0 .0 5 ) ;血浆 F ∶ C显著增加 (P<0 .0 1) ,血浆 F ∶ C明显下降 (P<0 .0 5 ) ,F 活性显著增加(P<0 .0 1) ,Fbg的活性显著增加 (P<0 .0 1) ;AT 活性显著降低 (P<0 .0 1)。结论 :ACI的发生与组织因子途径的启动有关 ,在 ACI早期患者血液呈高凝状态

关 键 词:脑梗死,急性 组织因子 组织因子途径抑制物 凝血酶原 因子Ⅶ促凝活性 因子Ⅷ促凝活性 纤维蛋白原 抗凝血酶Ⅲ
文章编号:1003-0603(2003)09-0529-03
修稿时间:2002-11-04

Observation on tissue factor pathway during the onset of acute cerebral infarction
WEN Zhibin ,XIONG Shilong ,HE Xiaofan ,HE Meixia ,HE Shilin ,XIE Qin zhi ,JIAN Zaifu ,CHE N Fangping ,XIAO Bo ,YANG Q idong . . Thrombosis and Hemostasis Lab. Observation on tissue factor pathway during the onset of acute cerebral infarction[J]. Chinese critical care medicine, 2003, 15(9): 529-531
Authors:WEN Zhibin   XIONG Shilong   HE Xiaofan   HE Meixia   HE Shilin   XIE Qin zhi   JIAN Zaifu   CHE N Fangping   XIAO Bo   YANG Q idong . . Thrombosis  Hemostasis Lab
Affiliation:Thrombosis and Hemostasis Lab, Department of Physiology, Xiangya Medical University, Central-South University, Changsha 410078, Hunan, China. wenzhibin2002@yahoo.com.cn
Abstract:OBJECTIVE: To establish the possible relationship between some coagulation factors and the onset of acute cerebral infarction (ACI). METHODS: The study population consisted of 71 patients with ACI confirmed by CT and 50 age-matched healthy volunteers. Blood samples were obtained during the onset period of ACI. Tissue factor (TF) and tissue factor pathway inhibitor (TFPI) activity in plasma were assayed with the chromogenic assay. Plasma TF and TFPI antigen were measured with enzyme linked immunoadsorbent assay (ELISA). Plasma F VII coagulation activity (F VII: C) and F VIII coagulation activity (F VIII: C) were developed in the one-stage system. Plasma prothrombin (FII) was determined with Ecarin assay. Plasma fibrinogen (Fbg) was measured with thrombin assay. Plasma antithrombin III activity (ATIII) was determined using heparin cofactor activity assay. RESULTS: Compared with the control, plasma TF activity and antigen in patients with ACI were significantly higher (both P<0.05). But plasma TFPI activity and antigen were remarkably lower in the ACI group (both P<0.05). Plasma F VII: C was significantly higher (P<0.01), and F VIII: C was markedly lower (P<0.05). Plasma FII was remarkably higher (P<0.01). Similarly the Fbg was significantly higher in the ACI than that in the control group (P<0.01), whereas ATIII was significantly lower (P<0.01). CONCLUSION: The initiation of TF pathway is contributed to the onset of ACI and the blood is in hypercoagulable state during the early period of ACI.
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