单核细胞组织因子在急性缺血性脑卒中的动态变化

目的观察急性缺血性脑卒中(AIS)患者急性期及恢复期组织因子(TF)的变化。方法选择发病48 h内的AIS患者30例为AIS组,健康体检者61例为对照组。采用RT-PCR检测单核细胞TF mRNA;采用ELISA法检测血浆TF抗原。结果与对照组比较,AIS组急性期患者单核细胞TF mRNA(0.254±0.04 vs 0.312±0.09)和血浆TF抗原[(197.18±94.91)ng/L vs(276.64±106.01)ng/L]均明显增高,呈同步上升趋势(P<0.05);与急性期比较,AIS组恢复期单核细胞TF mRNA及血浆TF抗原呈同步下降,差异均有统计学意义(P<0.05)。AIS组恢复期血浆TF抗原与对照组比较差异无统计学意义(P>0.05)。结论 AIS患者发作期血液呈高凝状态,血栓形成风险增加;动态观察AIS患者单核细胞TF mRNA与血浆TF抗原含量,对了解疾病的发生、发展有辅助作用。     

原发性高血压患者血浆组织因子途径的变化及降压治疗的影响

目的观察原发性高血压患者血浆组织因子途径、组织因子途径抑制物的变化及用依那普利、特拉唑嗪降压治疗后上述指标的变化.方法发色底物法、Ⅰ期凝固法检测1、2级原发性高血压患者55例、正常对照者28例的血浆组织因子(TF)、组织因子途径抑制物(TFPI)、FⅦC活性.55例高血压患者中27例接受依那普利治疗,28例接受特拉唑嗪治疗,疗程8周.结果原发性高血压患者血浆TF、FⅦC 、TFPI活性明显增高,与对照组相比差异有显著性(P<0.001);依那普利和特拉唑嗪治疗8周后血浆TF、FⅦC活性下降,与治疗前相比差异有显著性(P<0.001);两药均不影响TFPI的活性.结论原发性高血压患者血浆组织因子途径活性增加,依那普利和特拉唑嗪在有效降压的同时可通过调节组织因子途径的活性改善血栓前状态.     

血清瘦素与早发冠心病及血浆组织因子的关系

目的:探讨血清瘦素与早发冠心病及血浆组织因子的关系。方法:根据冠状动脉造影结果将200例患者分为早发冠心病组(120例)和对照组(80例)。应用酶联免疫吸附法(ELISA法)检测患者血清瘦素、血浆组织因子(TF)及组织因子途径抑制物(TFPI)水平。结果:早发冠心病组血清瘦素、血浆TF、TFPI及TF/TFPI值均高于对照组(均P<0.01);Pearson相关分析显示,血清瘦素水平与早发冠心病患者血浆TF、TFPI、TF/TFPI均呈正相关(均P<0.01);多元逐步回归显示,血清瘦素和早发冠心病患者血浆TF水平呈独立正相关(P<0.01)。结论:早发冠心病患者表现为高瘦素血症,高瘦素水平与TF的表达及早发冠心病的发生有关。     

冠心病患者血浆组织因子和组织因子途径抑制物的变化

目的 :通过检测不同类型冠心病 (CHD)患者血浆组织因子 (TF)和组织因子途径抑制物 (TFPI)水平变化 ,探讨其在CHD发病过程中的作用。方法 :以酶联免疫吸附测定法测定CHD患者血浆中TF和TFPI抗原水平。结果 :不稳定型心绞痛 (UAP)和急性心肌梗死 (AMI)患者的血浆TF和TFPI水平与正常对照者和稳定型心绞痛 (SAP)患者相比均有显著性增高 (P <0 .0 5 ) ,以AMI患者尤为明显 (P <0 .0 1) ;UAP和AMI患者的TF PI/TF比值显著降低 (P <0 .0 5 ) ,而SAP患者的上述指标与正常对照者相比 ,其差异均无显著性意义 (P >0 .0 5 )。结论 :UAP和AMI患者TFPI/TF系统失衡 ,标志高凝状态的存在 ;TF和TFPI在这两种类型CHD的发病机制中可能起着重要的作用     

维生素E对组织因子及其抑制物在冠心病中的干预作用

目的 :探讨冠心病 (CHD)的不同类型中血浆组织因子 (TF)及其抑制物 (TFPI)含量的差异变化及维生素E对急性心肌梗死 (AMI)干预作用。方法 :用ELISA方法检测CHD患者 [包括稳定型心绞痛 (SAP)、不稳定型心绞痛 (UAP)、AMI]入院时及治疗 2周时血浆TF、TFPI含量。结果 :①SAP组血浆TF、TFPI水平及TF/TF PI比值均高于正常对照组 ,但差异无统计学意义 (P >0 .0 5 ) ,且治疗前后无明显变化 (P >0 .0 5 )。②UAP组、AMI组血浆TF、TFPI水平及TF/TFPI比值明显高于正常对照组 ,差异有统计学意义 (P <0 .0 1) ,但两组常规治疗前后差异无统计学意义 (P >0 .0 5 )。③AMI加维生素E组干预治疗后TF值显著下降 (P <0 .0 1) ,与正常对照组比较差异无统计学意义 (P >0 .0 5 ) ,TFPI干预治疗后无明显变化 (P >0 .0 5 ) ,而TF/TFPI比值明显降低 (P <0 .0 1)。④各组TF与TFPI呈明显正相关 (P<0 .0 5 ,r=0 .4 32 )。结论 :TF及TFPI在CHD尤其是急性冠状动脉综合征的发生中起重要作用 ,维生素E的干预显著降低患者血浆TF水平 ,降低TF/TFPI比值而对TFPI无影响。     

冠心病患者凝血机制的变化及其临床意义

目的检测冠心病患者血浆组织因子(TF)、组织因子途径抑制物(TFPI)水平及国际标准化比值(INR)、活化部分凝血活酶时间(APTT)的变化,探讨其在冠心病诊治中的临床意义。方法冠心病患者96例(冠心病组),非冠心病患者25例(对照组),冠心病组分为急性心肌梗死组(33例)、不稳定性心绞痛组(33例)和稳定性心绞痛组(30例)。冠心病患者又按Gensini积分分为A组、B组和C组,每组32例。分析各组TF、TFPT、INR和APTT的变化。结果冠心病组患者TF、TFPI、TF/TFPI高于对照组,INR、APTT低于对照组;急性心肌梗死组患者TF、TFPI、TF/TFPI显著高于不稳定性心绞痛组及稳定性心绞痛组患者,INR、APTT明显低于不稳定性心绞痛组及稳定性心绞痛组患者。C组患者TF、TF/TFPI明显高于B组和A组,INR、APTT低于B组和A组患者;INR与TF/TFPI呈负相关(r=-0.302,P=0.003),INR与APTT呈正相关(r=0.349,P=0.01)。结论冠心病患者TF、TFPI、TF/TFPI、INR、APTT水平在一定程度上反映了病情的严重程度,其中TF/TFPI能反映冠心病患者的凝血状态,对冠心病患者的危险分层和治疗有一定的临床意义。     

原发性高血压患者血浆组织因子途径的变化及降压治疗的影响

目的 的发性高血压患者血浆组织因子途径，组织因子途径抑制物的变化及用依那普利，特拉唑嗪降压治疗后上述指标的变化。方法 发色底物法，I期凝固法检测1，2级原发性高血压患者55例，正常对照者28例的血乐组织因子（TF），组织因子途径抑制物（TFPI），FⅦ；C活性。55例高血压患者中27例接受依那普利治疗，28例接受特拉唑嗪治疗，疗程8周。结果 原发性高血压患者血浆TF，FⅦ：C，TFPI活性明显增高，与对照组相比差异有显著性（P＜0．001）；依那普利和特拉唑嗪治疗8周后血浆TF，FⅦ；C活性下降，与治疗前相比差异有显著性（P＜0．001）；两药均不影响TFPI的活性。结论 原发性高血压患者血浆组织因子途径活性增加，依那普利和特拉唑嗪在有效降压的同时可通过调节组织因子途径的活性改善血栓前状态。     

冠心病患者血浆组织因子、组织因子途径抑制物、白介素18、白介素10水平的变化及其关系

目的观察冠心病患者血浆组织因子(TF)、组织因子途径抑制物(TFPI)、白介素18(IL-18)、白介素10(IL-10)的变化,探讨其在冠心病(CHD)中的意义及其相互关系。方法 121例患者分为对照组(33例)与CHD组(96例),CHD组又分为急性心肌梗死(AMI)(33例),不稳定性心绞痛(UAP)(33例)和稳定性心绞痛(SAP)(30例)三个小组。采用酶联免疫吸附法分别测定血浆TF、TFPI、IL-18、IL-10的含量。结果 CHD组患者血浆TF、TFPI、TF/TFPI高于对照组,AMI小组患者血浆TF、TFPI、TF/TFP显著高于UAP及SAP小组患者,UAP小组患者高于SAP小组患者;CHD组患者血浆IL-18、IL-10、IL-18/IL-10高于对照组,AMI小组患者血浆IL-18、IL-18/IL-10显著高于UAP及SAP小组患者,UAP小组患者高于SAP小组患者;AMI和UAP小组患者血浆IL-10水平低于SAP小组患者;CHD组患者血浆TF与IL-18呈显著正相关(r=0.753,P=0.03),TF/TFPI与IL-18/IL-10呈正相关(r=0.496,P=0.01)。结论 CHD患者促凝因素和促炎症因子均显著升高,且与病情平行。促凝因子和促炎因子呈正相关,提示凝血因子和炎症因子在CHD发病中起重要作用,并可作为病情严重程度评价的参考指标。     

急性心肌梗死发作期间组织因子途径变化的观察

目的：观察急性心肌梗死（AMI）发作期间组织因子途径的变化。方法：69列临床确诊的AMI患和30例健康中老年人（作对照）被纳入研究对象。血浆中的组织因子（TF）和组织因子途径抑制物（TFPI）的活性测定采用发色底物法,TF和TFPI抗原采用ELISA法。激活的凝血因子Ⅶa采用重组可溶性TF法。凝血因子Ⅶ促凝活性采用活性测定法。结果：与对照组相比,AMI患血浆中TF、TFPI的活性均显增加[分别为5．67（1．77－54．95）mU/ml vs2.36(1.13-6.42)mU/ml,P＜0．01;224．85（86．65－512．12）％vs 138．75（51．72－297．2）％,P＜0．01]。同时TF、TFPI的抗原、凝血因子Ⅶa的活性亦有明显升高,但凝血因子Ⅶ促凝活性无显变化。结论：AMI发作期间体内组织因子途径被启动,血液呈现高凝状态。     

血浆凝血因子Ⅶ测定在冠心病中的临床意义

目的检测冠心病患者血浆中活化因子Ⅶ(FⅦa)、因子Ⅶ相关抗原(FⅦAg)与因子Ⅶ活性(FⅦC),探讨其临床意义。方法FⅦa采用重组可溶性组织因子法,FⅦAg采用ELISA法．FⅦC采用一期法测定。结果稳定型心绞痛组(30例)、不稳定型心绞痛组(20例)、急性心肌梗死(AMI)组(20例)FⅦa测定结果分别为(2．6±0．8)μg／L、(2．8±0．9)μg／L与(2．9±0．9)μg／L,均较对照组(40例)(2．2±0．7)μg／L为高(P＜0．05)。三组中FⅦa／FⅦAg分别为3．20、3．88与3．81,均较对照组(2．60)为高(P＜0．05),三组中的FⅦC仅稳定型心绞痛组增高(P<0．05),不稳定型心绞痛组降低(P<0．05),AMI组正常,而FⅦAg仅稳定型心绞痛组降低(P<0．05),其他组无明显改变。结论检测FⅦ评估冠心病及其危险事件的发生,以FⅦa、FⅦAg与FⅦC三项同时测定为好,而且用FⅦa绝对值及FⅦa／FⅦAg相对值作为高凝状态与危险因子比单测FⅦC更为可靠。     

慢性阻塞性肺疾病患者凝血功能异常与氧化应激的关系

目的 探讨慢性阻塞性肺疾病(COPD)急性加重(AECOPD)患者凝血功能异常与氧化应激的关系.方法 选28例AECOPD患者和30例健康对照者,检测其血浆中组织因子(TF)、组织因子途径抑制剂(TFPI)活性、总抗氧化能力(TAC)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-PX)活性及肺功能,并行动脉血气分析.结果 (1)与治疗前比较,AECOPD患者治疗后血浆TF、TFPI、TF/TFPI水平均明显下降(P<0.01),但仍高于健康对照者(P<0.01).(2)与治疗前比较,AECOPD患者治疗后血浆TAC、GSH-PX水平虽升高,但仍低于健康对照者;治疗后血浆MDA水平下降,但仍高于健康对照者(P<0.05).(3)相关分析:AECOPD患者治疗前TF/TFPI与血浆TAC、GSH-PX、PaO2呈负相关(r分别为-0.518、-0.454、-0.511;P<0.01,P<0.05,P<0.01),与中性粒细胞百分比呈正相关(r=0.379,P<0.05);而AECOPD患者治疗后TF/TFPI与血浆TAC、第1秒用力呼气容积占预计值百分比呈负相关(r分别为-0.420、-0.480;P值均小于0.05),与血浆MDA呈正相关(r=0.451,P<0.05).结论 AECOPD患者存在凝血/抗凝失衡及氧化/抗氧化失衡,凝血/抗凝失衡与氧化/抗氧化失衡之间存在显著相关性.

Abstract：

Objective To explore the relationship between coagulation/anticoagulation imbalance and oxidative stress in the patients with chronic obstructive pulmonary disease during acute exacerbation (AECOPD)before and after treatment.Methods Plasma tissue factor(TF)and tissue factor pathway inhibitor(TFPl)activity was detected by chromogenic assay in 28 AECOPD patients before and after treatment as well as in 30 healthy controls.The total antioxidative capacity(TAC),malondialdehyde (MDA)and gtutathione peroxidase(GSH-PX)in plasma were measured in both groups.Results The levels of plasma TF and TFPI,and their ratio(TF/TFPI)in AECOPD patients before treatment were significantly higher than those after treatment(all P<0.0 1),the latter were still higher than those in the healthy persons(all P<0.01).The levels of the TAC and GSH-PX in plasma in AECOPD patients before treatment were significantly lower than those after treatment(all P<0.01),the latter were still lower than those in the healthy persons(all P<0.01).The plasma MDA in AECOPD patients before treatment was significantly higher than that after treatment(P<0.0 1),which was still higher than that in the healthy persons(P<0.05).There were negative correlations between TF/TFPI ratio and TAC(r=-0.518.P<0.01),GSH-PX(r=-0.454,P<0.05),PaO2(r=-0.511,P<0.01)respectively and a positive correlation between TF/TFPI ratio and the percentage of neutrophils(r=0.379,P<0.05)in AECOPD patients before treatment.There still were negative correlations between TF/TFPI ratio and TAC (r=-0.420,P<0.05),FEV1% to predicted(r=-0.480,P<0.05)respectively,and a positive correlation between TF/TFPI ratio and MDA(r=0.45 1,P<0.05)in AECOPD patients after treatment.Conclusions There existed coagulation/anticoagulation imbalance and oxidation/antioxidation imbalance before and after treatment in AECOPD patients and their relationship was explored.     

组织因子及其抑制物在急性冠脉综合征中的作用研究

探讨急性冠脉综合征发生中血浆组织因子 (TF)及其抑制物 (TFPI)含量的动态变化及其血管紧张素转换酶抑制剂 (ACEI)captopril干预治疗的作用。用ELISA方法检测急性心肌梗塞 (AMI)不稳定心绞痛(UA)患者入院后即刻、第 1天、2天、3天、1周、2周、3周不同时间点血浆TF及TFPI的含量。 1 50例AMI患者中 ,AMI用ACEI干预治疗 (AMI +ACEI组 ) 2 5例 ,常规治疗组 (AMI组 ) 2 5例 ,UA组 2 8例 ,血浆TF、TFPI水平均明显高于正常对照组 (P <0 0 0 1)。AMI+ACEI组血浆TF水平发病后第 3天开始下降 ,于 2周时间点明显下降 ,同AMI组及UA组比较有显著的差异 (P <0 0 0 1)而较对照组比较差异无显著性 (P >0 0 5) ,AMI +ACEI组TFPI含量无明显下降 ,持续稳定在较高水平。 2 TF与TFPI呈正相关 (P <0 .0 1) (r=0 549)。组织因子及其抑制物在急性冠脉综合征中起重要作用。ACEI药物降低血浆TF水平对TFPI无影响 ,降低TF/TFPI比值     

Plasma tissue factor and tissue factor pathway inhibitor levels in patients with disseminated intravascular coagulation

We measured the plasma levels of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in patients with disseminated intravascular coagulation (DIC) to examine the relationship between TFPI and vascular endothelial cell injury. Plasma TF (273 ± 90 pg/ml) and TFPI (252 ± 125 ng/ml) levels were significantly increased in patients with DIC compared with non-DIC patients. Plasma TF antigen level was significantly increased in pre-DIC patients (285 ± 85 pg/ml), while the plasma TFPI level (152 ± 54 ng/ml) was not markedly increased in such a state. The plasma TF/TFPI ratio was high in the pre-DIC patients (2.10 ± 0.90), and low in the DIC patients (1.40 ± 0.87) and healthy volunteers (0.84 ± 0.26). There was no significant difference between the DIC patients with a good outcome and those with a poor outcome in terms of plasma TF levels, although the plasma TFPI level in the DIC patients with a good outcome (289 ± 133 ng/ml) was significantly higher than that in those with a poor outcome (187 ± 75 ng/ml). During the clinical course of DIC, plasma TF antigen was increased first, and an increase of the plasma TFPI level followed the increase in plasma TF level. These findings suggest that plasma TFPI is released from vascular endothelial cells and it may reflect vascular endothelial cell injury. It is conceivable that TF and TFPI may play an important role in the onset of DIC. © 1996 Wiley-Liss, Inc.     

Plasma tissue factor and tissue factor pathway inhibitor levels in patients with disseminated intravascular coagulation

We measured the plasma levels of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in patients with disseminated intravascular coagulation (DIC) to examine the relationship between TFPI and vascular endothelial cell injury. Plasma TF (273 ± 90 pg/ml) and TFPI (252 ± 125 ng/ml) levels were significantly increased in patients with DIC compared with non-DIC patients. Plasma TF antigen level was significantly increased in pre-DIC patients (285 ± 85 pg/ml), while the plasma TFPI level (152 ± 54 ng/ml) was not markedly increased in such a state. The plasma TF/TFPI ratio was high in the pre-DIC patients (2.10 ± 0.90), and low in the DIC patients (1.40 ± 0.87) and healthy volunteers (0.84 ± 0.26). There was no significant difference between the DIC patients with a good outcome and those with a poor outcome in terms of plasma TF levels, although the plasma TFPI level in the DIC patients with a good outcome (289 ± 133 ng/ml) was significantly higher than those with a poor outcome (187 ± 75 ng/ml). During the clinical course of DIC, plasma TF antigen was increased first, and an increase of the plasma TFPI level followed the increase in plasma TF level. These findings suggest that plasma TFPI is released from vascular endothelial cells and it may reflect vascular endothelial cell injury. It is conceivable that TF and TFPI may play an important role in the onset of DIC. Am. J. Hematol. 55:169–174, 1997. © 1997 Wiley-Liss, Inc.     

V617F JAK-2 mutation in patients with essential thrombocythemia: relation to platelet, granulocyte, and plasma hemostatic and inflammatory molecules

OBJECTIVE: This article evaluates patients with essential thrombocythemia (ET) to determine whether the V617F mutation in the JAK2 gene affects platelet hemostatic and adhesive molecules, platelet-polymorphonuclear leukocyte (PMN) interactions, and PMN-activation characteristics, as well as plasma hypercoagulation markers. PATIENTS AND METHODS: Thirty-seven ET patients with V617F JAK2 mutation and 38 wild-type, and 50 healthy controls were studied. RESULTS: Platelets from overall ET patients, compared to controls, expressed significantly higher membrane tissue factor (TF) and P-selectin (p < 0.01) and lower CD41 and CD42b (p < 0.01). TF appeared significantly higher in the V617F JAK2 carriers compared to wild-type, and total platelet TF antigen levels confirmed the same result. The presence of circulating platelet/PMN aggregates was significantly greater in the JAK2-mutation carriers than in the wild-type and controls (p < 0.05). PMN surface activation and inflammatory markers (i.e., CD14, TF, CD11b, and leukocyte alkaline phosphatase [LAP]) were all significantly higher in ET versus control subjects, with CD14 and LAP being the highest in the JAK2 mutation carriers. Finally, a significant increase in plasma hypercoagulation markers was found in ET patients, and the only difference for the V617F JAK2 carriers was higher plasma thrombomodulin levels (p < 0.01). Differences in white blood cell and PMN count, platelet TF, PMN CD14, and LAP, and plasma thrombomodulin remained significant after multivariate analysis. CONCLUSIONS: These results show that a correlation exists between the presence of V617F JAK2 mutation and selected hemostatic activation variables.     

缺血性心脑血管疾病患者血浆因子Ⅶ 水平及临床意义

目的系列测定缺血性心脑血管疾病患者血浆中凝血因子Ⅶ(FⅦ)的水平并探讨其临床意义。方法冠心病60例分为两组①血清胆固醇(TC)与甘油三酯(TG)正常组30例;②血清TC与TG增高组30例。缺血性脑卒中40例,分别采用重组可溶性组织因子法测定活化因子Ⅶ(FⅦ