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This study examined the changes of activities of vitamin K-dependent clotting factors (VKDCF) under various pathological conditions and explored the relationship between acquired deficiency of VKDCFs and hemorrhage. Clinical data of 35 patients who were diagnosed as having acquired deficiency of VKDCF were retrospectively analyzed. Coagulation factors involved in the intrinsic and extrinsic pathways were detected in these patients and 41 control subjects. The results showed that the average activities of VKDCFs were decreased in the patients in comparison to the control subjects and significantly increased after treatment of these patients with vitamin K and blood products. Multivariate regression analysis indicated that decreased activity of VKDCF was not an independent risk factor for bleeding disorders owing to deficiency or metabolic disturbance of vitamin K. It was concluded that acquired deficiency of VKDCF occurs under a variety of pathologic conditions and is closely associated with hemorrhagic events. Administration of vitamin K and transfusion of blood products containing high concentrations of VKDCFs helps alleviate the hemorrhagic diseases.
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Objective To investigate the adhesion molecule expression and functional status of platelets in lung cancer patients, and their relations with disease progression. Methods Using flow cytometry to measure the expression of surface antigens and functional status of platelets in 60 healthy control group, and 164 lung caneer patients. Results Comparing with control group, the expression in early group and mid term group(A group) of CD31, CD36, CD62, CD63 increased, and there is no significant meaning in the differences of surgery group (B group) of CD31, TSP, CD36, CD62, CD63. The expression in advanced group (C group) of CD31, TSP, CD36, CD62, CD63 increased. Comparing with A Group, the expression in B Group of CD36, CD62, CD63 decreased. The expression in C group of CD31, TSP, CD36, CD62, CD63 increased. Comparing with the small cell lung cancer, the expression of adenocareinorna of TSP, CD36,, CD62, CD63, squamous cell carcinoma of CD31, CD62, CD63, and alveolus cancer of CD31, TSP, CD63, all decreased. Conclusion The high level expression of platelet activation exists in patients with lung cancer of different stage, and decreased after operation. Platelet activation expressed significantly in the advanced stage of small cell lung cancer.
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Objective To evaluate the significance of TF-PCA to the diagosis of DIC by observing changes of tissue factor(TF) and procoagulant activity (PCA) in patients with disseminated inravaascular coagulation(DIC)according to the enhancenment degree of whole blood leukocyte-derived TF expression and TF-PCA stimulated by Lipopolysaccharide (LPS). Method Patients with acute leukemia (AL) were included during hospitalization from Jan. 2005 to Jan. 2007 in Union Hospital of Huazhong University of Science and Technology. Recalcification time of LPS-stimulated whole blood was applied to evaluate tissue factor clotting time (TiFaCT) : anticoagulated whole blood was incubated at 37°C for a certain time with or without LlS-stimulation, and then the recalcitication time was measured. TF-PCA were evaluated based on the decreased degree of whole blood mcalcification time(△s).LSI)- t test and bivariate correlation analysis were analyzed by using the SPSS software package (version 13.0 for Windows). A P-value less than 0.05 was considered statistically significant. Results A retrospective and contrast analysis indicated that △s in patients with DIC and patients suspected with DIC were (95.2±68.6) and (85.8±16.9), respectively. When compared with normal controls(30.4±25.1 ), the difference both had extremely statistical significe(P<0.01). The results of TF mRNA detection and TF-PCA inhibitory experiments showed that the method of TiFaCT had a high sersitivity and specificity for determination of TF-PCA. Condusiots The levels of TF-PCA were obviously elevated after stimulated by LPS in patients with DIC or suspected with DIC.TiFaCT has an important clinical reference value for the diagnostic and prognostic evaluation of DIC.
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Objective To observe the changes of coagulation function in patients with acute lowerlimb deep venous thrombosis(DVT)and evaluate the risk factors for DVT. Methods Plasma APTT.PT,TT,D-dimer and fibrinogen(Fbg)were detected by an automated coagulation analyzer in 62 acute lower-limb DVT patients and 70 controls:Retrospective studies on the clinical data of all patients were done by binary logistic regression analysis.Results (1)In DVT group,plasma APTT,PT and TT,the levels of D-dimer and fibrinogen.and D-dimer/fibrinogen ratio(D/F ratio)were higher when compared with control group(au P＜0.01);(2)There were positive correlations between D-dimer and fibrinogen both in DVT and control groups(r=0.475,P＜0.01;r=0.564,P＜0.01,respectively);(3)Logistic analysis indicated that acute lower-limb DVT was associated with the presence of hypertension and increased plasma level of fibrinogen(OR=24.99,P＜0.01: OR=4.346.P＜0.01,respectively).Conclusions Hypertension and elevated plasma level of fibrinogen are independent risk factors for acute lower-limb DVT.
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A new, convenient, and rapid method for kinetic measurement of human fibrinolysis was established. The alteration of absorbance (A) in the process of blood coagulation and lyses was automatically scanned and recorded using a UV2000 spectrophotometer connected to a computer. The parameters of human fibrinolysis kinetics were established. Urokinase at 20 U/mL was the optimal concentration used. There was significant difference in fibrinolysis kinetics and plasma plasminogen concentration between 22 normal subjects and 27 patients with acute myeloblastic leukemia (P＜0.05 and ＜0.01 respectively). The coefficience of variation was (5.24±1.51)%. This method could also be used to measure the plasma fibrinogen concentration at the same time. It was concluded that this method was stable and was capable of providing dynamic, direct experimental data and multiparemeters for clinicians. It was also valuable in evaluating the anti- and pro-fibrinolytic capcity of patients' plasmas, allowing for monitoring of therapy, choice of drugs and adjustment of drug concentrations.
ABSTRACT
A new, convenient, and rapid method for kinetic measurement of human fibrinolysis was established. The alteration of absorbance (A) in the process of blood coagulation and lyses was automatically scanned and recorded using a UV2000 spectrophotometer connected to a computer. The parameters of human fibrinolysis kinetics were established. Urokinase at 20 U/mL was the optimal concentration used. There was significant difference in fibrinolysis kinetics and plasma plasminogen concentration between 22 normal subjects and 27 patients with acute myeloblastic leukemia (P<0.05 and <0.01 respectively). The coefficience of variation was (5.24+/-1.51)%. This method could also be used to measure the plasma fibrinogen concentration at the same time. It was concluded that this method was stable and was capable of providing dynamic, direct experimental data and multiparemeters for clinicians. It was also valuable in evaluating the anti-and pro-fibrinolytic capcity of patients' plasmas, allowing for monitoring of therapy, choice of drugs and adjustment of drug concentrations.
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To study the variation and significance of plasma coagulation factor Ⅶ (FⅦ) in differ ent kinds of ischemia heart disease (IHD) and examine its relation with plasma lipid and gene polymorphism. FⅦa was determined with one stage clotting assay by using a recombinant soluble tissue factor (rsTF). FⅦc was measured with one stage clotting assay. FⅦag was quantified with an enzyme-linked immunosorbent assay (ELISA). Polymorphism was analyzed with PCR-urea-polyacrylamide gel electrophoresis. Our results showed that FⅦa in stable angina (SA),unstable angina (UA), obsolete and acute myocardial infraction (OMI, AMI) patients was higher than those of normal group with the differences being significant within any two groups. FⅦag in UA, OMI and AMI was higher than those in SA and normal groups. There were positive correlations between FⅦa and serum triglycerides, FⅦa and FⅦc, FⅦc and FⅦag. FⅦ-323 0/10 bp polymorphism analysis was performed in 60 patients and 0/10 bp polymorphism was found in 5 cases. FⅦc and FⅦag were much lower in cases of 0/10 bp groups than those in cases of 0/0 bp groups. It is concluded that there was activation of extrinsic coagulation pathway in every kind of IHD to different extent. FⅦa was the risk factor in the development of IHD, and more sensitive in reflecting the severity of cardiovacutar disease than FⅦc or FⅦag. FⅦa was higher in OMI, which may be one of the risk factors of re-infraction. Serum triglyceride may indirectly lead to the development of IHD by increasing the level of FⅦa. FⅦ-323 0/10 bp polymorphism was present in Chinese patients with IHD and it was correlated with the level of FⅦc, FⅦag in plasma. 10 bp allelomorphic gene was a protective factor against thrombogenesis.
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To study the variation and significance of plasma coagulation factor VII (FVII) in different kinds of ischemia heart disease (IHD) and examine its relation with plasma lipid and gene polymorphism. FVIIa was determined with one stage clotting assay by using a recombinant soluble tissue factor (rsTF). FVIIc was measured with one stage clotting assay. FVIIag was quantified with an enzyme-linked immunosorbent assay (ELISA). Polymorphism was analyzed with PCR-urea-polyacrylamide gel electrophoresis. Our results showed that FVIIa in stable angina (SA), unstable angina (UA), obsolete and acute myocardial infraction (OMI, AMI) patients was higher than those of normal group with the differences being significant within any two groups. FVIIag in UA, OMI and AMI was higher than those in SA and normal groups. There were positive correlations between FVIIa and serum triglycerides, FVIIa and FVIIc, FVIIc and FVIIag. FVII-323 0/10 bp polymorphism analysis was performed in 60 patients and 0/10 bp polymorphism was found in 5 cases. FVIIc and FVIIag were much lower in cases of 0/10 bp groups than those in cases of 0/0 bp groups. It is concluded that there was activation of extrinsic coagulation pathway in every kind of IHD to different extent. FVIIa was the risk factor in the development of IHD, and more sensitive in reflecting the severity of cardiovacutar disease than FVIIc or FVIIag. FVIIa was higher in OMI, which may be one of the risk factors of re-infraction. Serum triglyceride may indirectly lead to the development of IHD by increasing the level of FVIIa. FVII-323 0/10 bp polymorphism was present in Chinese patients with IHD and it was correlated with the level of FVIIc, FVIIag in plasma. 10 bp allelomorphic gene was a protective factor against thrombogenesis.
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The plasma levels of inflammatory cytokine interleukin-6 (IL-6) and anti-inflammatory cytokine interleukin-10 (IL-10) in the patients with unstable angina or stable angina were determined and compared. In 30 patients with unstable angina and 22 patients with stable angina, plasma levels of IL-10 and IL-6 were detected by ELISA and plasma lipid parameters by lipid research clinical methods respectively. The results showed plasma levels of IL-10 were significantly lower in unstable angina group than in stable angina group (P=0. 005), while those of IL-6 were significantly increased in unstable angina group as compared with those in stable angina group (P = 0. 039).There was a significantly negative correlation between IL-10 and IL-6 in patients with unstable angina (r=-0.41, P=0. 003). In the unstable angina group, IL-6 levels were obviously positively correlated with TC (r=0. 314, P=0. 023), but not with TG and HDL. There were no significant correlations between IL-10 and plasma lipid parameters. It was suggested that the decreased IL-10and increased IL-6 might be associated with the atheromatous plaque stability and progression of coronary heart diseases. IL-10 may play an important role in preventing coronary vascular lesions.
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The plasma levels of inflammatory cytokine interleukin-6 (IL-6) and anti-inflammatory cytokine interleukin-10 (IL-10) in the patients with unstable angina or stable angina were determined and compared. In 30 patients with unstable angina and 22 patients with stable angina, plasma levels of IL-10 and IL-6 were detected by ELISA and plasma lipid parameters by lipid research clinical methods respectively. The results showed plasma levels of IL-10 were significantly lower in unstable angina group than in stable angina group (P = 0.005), while those of IL-6 were significantly increased in unstable angina group as compared with those in stable angina group (P = 0.039). There was a significantly negative correlation between IL-10 and IL-6 in patients with unstable angina (r = -0.41, P = 0.003). In the unstable angina group, IL-6 levels were obviously positively correlated with TC (r = 0.314, P = 0.023), but not with TG and HDL. There were no significant correlations between IL-10 and plasma lipid parameters. It was suggested that the decreased IL-10 and increased IL-6 might be associated with the atheromatous plaque stability and progression of coronary heart diseases. IL-10 may play an important role in preventing coronary vascular lesions.
Subject(s)
Angina, Unstable/blood , Interleukin-10/blood , Interleukin-6/bloodABSTRACT
BACKGROUND: The elevation of plasma fibrinogen(Fbg) is a key risk factor of cerebrovascular diseases. The evaluation of the monomer polymerization function of fibrin has even more important clinical merit than the detection of Fbg level.OBJECTIVE: To investigate the clinical significance of the monomer polymerization function of fibrin in patients with isehemie cerebrovascular diseases and its impacts on rehabilitative intervention.DESIGN: A case control study employing patients and healthy individual as subjects.SETTING: An Institute of Hematology and Department of Neurology of one university.PARTICIPANTS: Totally 110 patients with different ischemic cerebrovascular disease selected from the Department of Neurology, Union Hospital of Tongji Medical College, Huazhong Science and Technology University from September 2001 to March 2002, and 50 healthy individuals were included in the study.METHODS: Rehabilitative intervention was performed in 31 randomly selected cerebral infarct patients, and the parameters indicating the monomer polymerization functions of fibrin in the plasma were detected by the measurement system for the monomer polymerization function of fibrin.MAIN OUTCOME MEASURES: Abnormal condition of monomer polymerization function of fibrin in each parameter.RESULTS: Each parameter indicating the monomer polymerization functions of fibrin in plasma was significantly increased in ischemic cerebrovascular diseases patients than healthy individuals( P ＜ 0.01 ) . The abnormal rate of Fbg leveland fibrin monomer polymerization velocity (FMPV) was significantly elevated in ischemic cerebrovascular disease patients than healthy individuals ( P ＜ 0. 01 ) . The relative risk(RR) of ischemic cerebrovascular diseases in patients with abnormal FMP functions was 4 to 31 times more than healthy control group. In cerebral infarct group, FMPV of anterior circulation infarct subgroup was significantly elevated than that of posterior circulation infarct and lacunar cerebral infarct subgroups( P ＜ 0.05). The FMP function of anterior cerebral infarct patients was significantly higher than that of healthy group before rehabilitative intervention. Although each FMP parameter reduced after rehabilitative intervention, the difference between was not significant compared with that of before therapy.CONCLUSION: FMP function analysis can completely and objectively reflect the coagulation status of the patients with ischemic cerebrovascular diseases, and it can also reflect the range and severity of infarct to some extent. Although common rehabilitative intervention cannot effectively improve the high-coagulation of the blood, the impacts of specific rehabilitative intervention on the coagulation mechanism deserve further investigation.
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BACKGROUND: Microsurgical operation might fail due to trauma-induced hypercoagulability.OBJECTIVE: To observe the changes of polymerization of fibrin monomer after the treatment of trauma so as to explore an effective means for assisting the prediction of post-traumatic hypercoagulability and thrombosis.DESIGN: Case-control observation and self-control study.SETTING: Institute of Thrombus and Hemostasis, the Union Hospital affiliated to Tongji Medical College of Huazhong University of Science and Technology.PARTICIPANTS: Totally 34 traumatic patients were included from those who were admitted to the Union Hospital affiliated to Tongji Medical College, Huazhong University of Science and Technology, between May 2001 and January 2002. There were 18 males and 16 females aged 8-65 years old. Another 96 healthy people, 50 males and 46 females aged 21-68 years old, who came for routine physical examination were enrolled as normal controls. The history of coagulation impairment, and general and coagulation-related diseases were excluded in all the subjects.METHODS: Polymerization of plasmic fibrin monomer was detected. Fibrinogen would transform into fibrin monomers and display polymerization induced by acutobin. The accompanied changes of the turbidity were dynamically monitored using spectrophotometer at 340 nm; the obtained electrical signals were then input into the computer for statistical analysis. Venous blood samples were collected from traumatic patients immediately after hospitalization and on the 3rd day after the treatment with clinical debridement, surgery, sutures, liquid supplement and administration of antibiotics to determine polymerization of fibrin monomer. MAIN OUTCOME MEASURES: ① The rate of polymerization of fibrin monomer (taken as the comprehensive predictor for the concentration and function of plasmic fibrinogens). ② Maximum absorbency (reflecting the amount of coagulable plasmic fibrinogen in blood specimen). ③ The ratio between the rate of polymerization of fibrin monomer and maximum ab sorbency (reflecting the polymerization of plasmic fibrinogen molecules). RESULTS: All participants completed the corresponding examinations and were brought into data analysis. ① In traumatic group, the rate of fibrin monomer polymerization, the content of fibrinogen, the ratio of polymerization rate to maximum absorbency were all significantly higher than those in normal control group [traumatic group: 0.87±0.31, (5.81±3.22) g/L,4.61±0.97; normal control group: 0.61±0.15, (3.36±1.02) g/L, 3.93±0.68,P ＜ 0.01]. ② At treatment of 3 days, although the rate of polymerization and the content of fibrinogen were found slightly declined, they were still higher than those in normal group [3.93±0.68, (4.21±1.93) g/L]; however,the ratio of polymerization rate to maximum absorbency did not change after treatment (4.68± 1.19).CONCLUSION: The content and function of fibrinogen would increase in traumatic patients. Traumatic patients display hypercoagulability characteristics and have thrombosis tendency. Determining the polymerization of fibrin monomer can be taken as an effective means for assisting the prediction of posttraumatic hypercoagulability and thrombosis.
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Objective To study the role of focal adhesion kinase in the breast carcinoma cell adhesion and migration mediated by coagulation factor Ⅶa combined with tissue factor to explore the mechanism of tissue factor promoting metastasis. Methods The count of adherent cells were detected by using colorimetric assay,cell migration was detected with modified Bodyen chamber,and the FAK and the tyrosine phosphorylation of FAK were detected by immunoprecipitation and Western blot.Results Factor Ⅶa combinaed with tissue factor induced the tyrosine phosphorylation of FAK,which took part in the cancer cell's migration.Conclusion FAK is an important message of the breast carcinoma's adhesion and migration mediated by TF.
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In order to investigate the association of fibrin monomer polymerization function (FMPF) with traditional cerebrovascular risk factors and ischemic cerebrovascular disease in old people, 1:1 paired case-control comparative study was performed for FMPF and traditional cerebrovascular risk factors on 110 cases of old ischemic cerebrovascular disease and 110 controls matched on age, sex and living condition. The results showed that cerebrovascular risk factors were more prevalent in case group than in control group. In the case group, FMPF was significantly higher than in control group. There was a significant positive correlation between hypertension and fibrin monomer polymerization velocity (FMPV), hypertension and fibrinogen (Fbg), alcohol consumption and Fbg, but no significant correlation between diabetic mellitus, smoking and FMPF was found. Among the parameters of blood lipids, there were significant positive correlations between total cholesterol (TC) and parameters of FMPF to varying degrees, triglycerides (TG) and FMPV, TG and Fbg. Our results also showed there were significant linear trends between TC and FMPV (P < 0.001), TC and Fbg (P = 0.0087), TG and FMPV/Amax (maximum absorbance) (P = 0.0143) respectively. Multiple logistic regression analysis revealed that FMPF in case group remained significantly higher than control group after adjustment of all risk factors that were significant in univariate analysis. It was concluded that there is a possible pathophysiological link between FMPF and cerebrovascular risk factors. An elevated FMPF is associated with ischemic cerebrovascular disease and an independent risk factor of this disease. In old people, detection of FMPF might be a useful screening to identify individuals at increased cerebrothrombotic risk.
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Case-Control Studies , Cerebral Infarction , Blood , Cerebrovascular Disorders , Blood , Fibrin Fibrinogen Degradation Products , Metabolism , Hypertension , Logistic Models , Polymers , Risk FactorsABSTRACT
In order to further investigate the effect of annexin II (Ann-II) on tissue plasminogen activator (t-PA)-dependent plasminogen (PLG) activation and its interactive mechanism, recombinant native Ann-II bound t-PA, PLG and plasmin with high affinity was examined. The flow cytometric assay showed that the ann-II expression rate was higher in the human umbilical vein endothelial cell (HUVEC) (87.65%) than in the HL-60 cells as controls (35.79%). Two irrelevant proteins, bovine serum albumin (BSA) and equine IgG (EIG) had no effect on the production of plasmin. Ann-II-mediated enhancement of t-PA-dependent PLG activation was inhibited by epsilon-aminocaproic acid or by pretreatment of Ann-II with carboxypeptidase B with the inhibitive rate being 77.8% and 77.0%, respectively. It was revealed that the effect of Ann-II on PLG activation was specific for t-PA. Urokinase didn't bind to Ann-II, demonstrating the role of receptor-related lysine residues on activation of PLG, showing that the Ann-II-PLG interaction was dependent upon carboxyl-terminal lysine residues. These findings suggest that annexin II-mediated co-assembly of t-PA and PLG may promote plasmin generation and play a key role in modulating fibrinolysis on the endothelial surface.
Subject(s)
Humans , Annexin A2 , Pharmacology , Cells, Cultured , Endothelium, Vascular , Cell Biology , Metabolism , Fibrinolysis , Plasminogen , Metabolism , Recombinant Proteins , Pharmacology , Tissue Plasminogen Activator , Metabolism , Umbilical Veins , Cell BiologyABSTRACT
In order to study the role of annexin II, a recombinant expression vector, pZeoSV2(+) ANN II, containing the annexin II cDNA, was developed. The 1.1-kb-length annexin II cDNA was inserted into a expression vector, PZeoSV(+) and transfected into HL-60 cells which had low baseline expression of Ann- II. pZeoSV(+) ANN II was analyzed by restriction mapping and the Ann- II sequence identified. The ability of the transfected cells, non-transfected and mock-transfected cells to stimulate t-PA-depend plasminogen activation was compared. The results showed that HL-60 with pZeoSV(+) ANN II transfection could significantly increase the plasminogen activation (8.9 +/- 1.2 U) in vitro with the difference being significant as compared with non-transfected (1.5 +/- 0.4 U) and mock-transfected cells (4.2 +/- 0.9 U), respectively. Antiannexin II oligonucleotides significantly inhibited the binding ability of t-PA and plasminogen to annexin II, and obviously reduced the plasminogen activation in vitro. The above findings showed human umbilical vein endothelial cells (HUVECs) treated with sense or missense oligonucleotides indicated no significant change in binding of t-PA and PLG. Treatment of HUVECs with antiannexin II oligonucleotides could significantly reduce the plasminogen activation by 2.4 +/- 0.3 U as compared with sense oligonucleotide group in binding of t-PA and PLG. These results, therefore, suggest that Ann- II can bind plasminogen and participate in the stimulation of t-PA-dependent activation of plasminogen, and that interference with Ann-II mRNA by antisense oligonucleotide may be a new strategy for the therapy of bleeding in patients with hyperfibrinolysis.
Subject(s)
Humans , Annexin A2 , Genetics , Metabolism , Physiology , DNA, Complementary , Genetics , Endothelium, Vascular , Cell Biology , HL-60 Cells , Pathology , Oligonucleotides, Antisense , Genetics , Metabolism , Plasminogen , Metabolism , RNA, Messenger , Genetics , Metabolism , Physiology , Receptors, Cell Surface , Metabolism , Recombinant Proteins , Genetics , Metabolism , Tissue Plasminogen Activator , Metabolism , Transfection , Umbilical Veins , Cell BiologyABSTRACT
In order to further investigate the effect of annexin II (Ann-II) on tissue plasminogen activator (t-PA)-dependent plasminogen (PLG) activation and its interactive mechanism, recombinant native Ann-II bound t-PA, PLG and plasmin with high affinity was examined. The flow cytometric assay showed that the ann-II expression rate was higher in the human umbilical vein endothelial cell (HUVEC) (87.65%) than in the HL-60 cells as controls (35.79%). Two irrelevant proteins, bovine serum albumin (BSA) and equine IgG (EIG) had no effect on the production of plasmin. Ann-II-mediated enhancement of t-PA-dependent PLG activation was inhibited by epsilon-aminocaproic acid or by pretreatment of Ann-II with carboxypeptidase B with the inhibitive rate being 77.8% and 77.0%, respectively. It was revealed that the effect of Ann-II on PLG activation was specific for t-PA. Urokinase didn't bind to Ann-II, demonstrating the role of receptor-related lysine residues on activation of PLG, showing that the Ann-II-PLG interaction was dependent upon carboxyl-terminal lysine residues. These findings suggest that annexin II-mediated co-assembly of t-PA and PLG may promote plasmin generation and play a key role in modulating fibrinolysis on the endothelial surface.
Subject(s)
Annexin A2/pharmacology , Cells, Cultured , Endothelium, Vascular/cytology , Endothelium, Vascular/metabolism , Fibrinolysis , Plasminogen/metabolism , Recombinant Proteins/pharmacology , Tissue Plasminogen Activator/metabolism , Umbilical Veins/cytologyABSTRACT
AIM: To study the expression of tissue factor (TF) in cerebral microvascular thrombosis and its dynamic changes in rats. METHODS: 50 female SD rats were randomized to control group, 2, 4, 6, and 24 hours after thrombosis groups, 10 rats in each group. The model of cerebral microvascular thrombosis was induced by photo-chemical method. ELISA and immunohistochemistry methods were used to observe the changes of TF contents in blood plasma and the expression of TF in cerebral microvascular in each group. RESULTS: Cerebral thrombosis was induced by photo-chemical method successfully. The TF content in plasma was obviously higher in 4 h and 6 h groups than that in control group (P