细胞黏附因子对深静脉血栓形成的影响及中药干预机制的研究
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摘要
目的:从细胞黏附因子的角度,深入探讨深静脉血栓形成(DVT)的本质,并探讨中药干预DVT中细胞黏附因子的作用机制,为临床诊治提供客观依据。
方法:临床筛选急性期DVT患者60例,按中医证型分为湿热下注型、血瘀湿重型,观察血清ICAM-1,VCAM-1,PSGL-1的水平,探讨性别及临床分型间是否存在差异,并统计三个指标间的相关性。实验研究以下腔静脉结扎法大鼠为模型,采用中药消栓通脉颗粒为治疗组,血府逐瘀胶囊、穿王消炎片、肝素钠、生理盐水为对照组。观察各组大鼠血清ICAM-1水平以及下腔静脉病理形态学改变,及静脉壁中炎性细胞、VCAM-1、PSGL-1的表达。
结果:临床研究显示DVT患者的血清ICAM-1、VCAM-1、PSGL-1均升高(P<0.01),湿热下注型较血瘀湿重型患者明显升高(P<0.01),性别间比较差异无显著性(P>0.05)。同组间混合型患者血清细胞黏附因子明显高于中央型、周围型,有显著性差异(P<0.05,P<0.01);中央型患者平均水平高于周围型,比较差异无显著性(P>0.05)。实验研究显示血栓模型组大鼠下腔静脉病理形态学改变较假手术组严重,血清ICAM-1水平以术后第1天最高,随天数增加逐渐下降;静脉壁中VCAM-1、PSGL-1表达以术后第3天最明显;在术后第1天炎性细胞以中性粒细胞为主,术后第3、6天以淋巴细胞、单核细胞为主;结果显示消栓通脉颗粒能明显改善大鼠下腔深静脉血栓形成的病理改变程度,降低血清ICAM-1水平,减少静脉壁中炎性细胞、VCAM-1、PSGL-1的表达(P<0.05,P<0.01)。
结论:细胞黏附因子参与了DVT的发生、发展及机化、消退整个过程,并可做为中医临床辨证的客观指标之一,而中药可以通过干预细胞黏附因子的角度来达到治疗DVT的目的。
Objective:To investigate the pathogenesis of deep vein thrombosis(DVT) from the view of cell adhesion molecules(CAMs) and interventional mechanism of Chinese Herbs on DVT,in order to provide objective basis for clinical diagnosis and treatment.
Methods:60 patients of DVT were divided into groups according to the syndrome differentiation type of traditional Chinese medicine(TCM) respectively.Based on the type of TCM,it was divided into the syndrome of pathogenic dampness-heat(A), the syndrome of blood stasis and dampness(B), 20 health people as control(C). All patients and healths were determined blood serum levels of ICAM-1, VCAM-1,PSGL-1,and discuss whether there is difference in the point of gender and traditional medical syndrome.In the experiment, 180 Wistar rats were divided into six groups which included Xiao Shuan Tong Mai group, Xue Fu Zhu Yu capsule group, Chuan Wang Xiao Yan tablets group, Haperin group,model group, sham group.Then to observe the pathological character, the serum level of ICAM-1 and the expression of the inflammation cells,VCAM-1,PSGL-1 in the vein walls.
Results:The serum levels of ICAM-1,VCAM-1,PSGL-1 of patients were higher than those of the control(P<0.01).The serum levels of ICAM-1,VCAM-1,PSGL-1 in group A were higher than group B and C(P<0.01),there is no distinct difference in the point of gender(P>0.05).The level of blood serum of CAMs of mixed type is higher than that of center type and around type(P<0.05,P<0.01).The level of CAMs of center type is higher than around type,but there is no obviously difference(P>0.05).Experiment shows that pathological changes in models were more severe than sham, higher levels of VCAM-1,PSGL-1 and higher expressions of the inflammation cells in the vein wall(P<0.05,P<0.01).The level of blood serum CAMs is maximal on the first day after operation,and then declined gradually.Xiao Shuan Tong Mai can effectively improved the pathological changes, reduced the expressions of these CAMs and inflammatory cytokines(P<0.05,P<0.01 ).
Conclutions:CAMs may participate in all pathological courses of DVT which involved in genesis,development,organization and recanalization. It can be as one of the objective index in the syndrome type of TCM.
The mechanism of the treatment of DVT by Chinese herbs may be the intervention and modulation of the CAMs.
方法:临床筛选急性期DVT患者60例,按中医证型分为湿热下注型、血瘀湿重型,观察血清ICAM-1,VCAM-1,PSGL-1的水平,探讨性别及临床分型间是否存在差异,并统计三个指标间的相关性。实验研究以下腔静脉结扎法大鼠为模型,采用中药消栓通脉颗粒为治疗组,血府逐瘀胶囊、穿王消炎片、肝素钠、生理盐水为对照组。观察各组大鼠血清ICAM-1水平以及下腔静脉病理形态学改变,及静脉壁中炎性细胞、VCAM-1、PSGL-1的表达。
结果:临床研究显示DVT患者的血清ICAM-1、VCAM-1、PSGL-1均升高(P<0.01),湿热下注型较血瘀湿重型患者明显升高(P<0.01),性别间比较差异无显著性(P>0.05)。同组间混合型患者血清细胞黏附因子明显高于中央型、周围型,有显著性差异(P<0.05,P<0.01);中央型患者平均水平高于周围型,比较差异无显著性(P>0.05)。实验研究显示血栓模型组大鼠下腔静脉病理形态学改变较假手术组严重,血清ICAM-1水平以术后第1天最高,随天数增加逐渐下降;静脉壁中VCAM-1、PSGL-1表达以术后第3天最明显;在术后第1天炎性细胞以中性粒细胞为主,术后第3、6天以淋巴细胞、单核细胞为主;结果显示消栓通脉颗粒能明显改善大鼠下腔深静脉血栓形成的病理改变程度,降低血清ICAM-1水平,减少静脉壁中炎性细胞、VCAM-1、PSGL-1的表达(P<0.05,P<0.01)。
结论:细胞黏附因子参与了DVT的发生、发展及机化、消退整个过程,并可做为中医临床辨证的客观指标之一,而中药可以通过干预细胞黏附因子的角度来达到治疗DVT的目的。
Objective:To investigate the pathogenesis of deep vein thrombosis(DVT) from the view of cell adhesion molecules(CAMs) and interventional mechanism of Chinese Herbs on DVT,in order to provide objective basis for clinical diagnosis and treatment.
Methods:60 patients of DVT were divided into groups according to the syndrome differentiation type of traditional Chinese medicine(TCM) respectively.Based on the type of TCM,it was divided into the syndrome of pathogenic dampness-heat(A), the syndrome of blood stasis and dampness(B), 20 health people as control(C). All patients and healths were determined blood serum levels of ICAM-1, VCAM-1,PSGL-1,and discuss whether there is difference in the point of gender and traditional medical syndrome.In the experiment, 180 Wistar rats were divided into six groups which included Xiao Shuan Tong Mai group, Xue Fu Zhu Yu capsule group, Chuan Wang Xiao Yan tablets group, Haperin group,model group, sham group.Then to observe the pathological character, the serum level of ICAM-1 and the expression of the inflammation cells,VCAM-1,PSGL-1 in the vein walls.
Results:The serum levels of ICAM-1,VCAM-1,PSGL-1 of patients were higher than those of the control(P<0.01).The serum levels of ICAM-1,VCAM-1,PSGL-1 in group A were higher than group B and C(P<0.01),there is no distinct difference in the point of gender(P>0.05).The level of blood serum of CAMs of mixed type is higher than that of center type and around type(P<0.05,P<0.01).The level of CAMs of center type is higher than around type,but there is no obviously difference(P>0.05).Experiment shows that pathological changes in models were more severe than sham, higher levels of VCAM-1,PSGL-1 and higher expressions of the inflammation cells in the vein wall(P<0.05,P<0.01).The level of blood serum CAMs is maximal on the first day after operation,and then declined gradually.Xiao Shuan Tong Mai can effectively improved the pathological changes, reduced the expressions of these CAMs and inflammatory cytokines(P<0.05,P<0.01 ).
Conclutions:CAMs may participate in all pathological courses of DVT which involved in genesis,development,organization and recanalization. It can be as one of the objective index in the syndrome type of TCM.
The mechanism of the treatment of DVT by Chinese herbs may be the intervention and modulation of the CAMs.
引文
[1] Lindblad B,Sternby NH,Bergqvist D.Incidence of venous thromboembolism verified by necrospy over 30 years[J].BMJ,1991;302(6778):709-711.
[2] Collins LM.DeepVenousThrombosis[J].Nurse Pract Forum,1998(3):163-169.
[3] Roumen Klappe EM,Den Heijer M,Van Uum SH,et al.Inflammatory response in the acute phase of deep vein thrombosis[J].J Vasc Surg,2002;35(4):701-706.
[4] Eftychiou V.Clinical diagnosis and management of the patient with deep venous thromboembolism and acute pulmonary embolism[J].Nurse Pract,1996;21(3):50-62.
[5] Fowkes FJ,Price JF,Fowkes FG..Incidence of diagnosed deep vein thrombosis in the general population:systematic review[J].Eur J Vasc Endovasc Surg 2003;25(1):1–5.
[6] Kahn SR.The clinical diagnosis of deep venous thrombosis:integrating incidence, risk factors,and symptoms and signs[J].Arch Intern Med,1998;15(21):2315–2323.
[7] Kakkar VV,Lawrence D.Hemodynamic and clinical assessment after therapy for acute deep vein thrombosis.A prospective study[J].Am J Surg,1985;15(4A):54-63.
[8] Coon WW.Venous thromboembolism.Prevalence,risk factors,and prevention[J].Clin Chest Med,1984;5(3):391-401.
[9] Ross R.The pathogenesis of atherosclerosis:a perspective for the 1990s[J].Nature 1993;62(29):801.
[10] Rosenson Rs,Tangeney CC.Antiathero thrombotic properties of stains::implications for cardiovascular event reduction [J].JAMA 1998;279::1643-50.
[11] Peterk,Weirich U,NordtTK, etal.Soluble vascular cell adhesion molecule- 1(VCAM-1) as potential marker of atherosclerosis[J].Thromb Haemost. 1999;82 Suppl 38-43.
[12] WuY,ZhuBD.Effect of DangguiBuxue Decoctiononpro-liferation and expre- ssion of intercellular adhesion molecule-1 in human umbilicalvein endothelialcells[J]. West China Univ Med Sci,2001,32(4):593-595.
[13] ZhangYJ,ZhaoLG,WuXZ.Effect of HuoxuehuayuDe–coctionon expression of adhe-sive molecular of intrapulmon icendothelial cell of rat suffered fromSAP[J].China Tradit Herb Drugs,2001,32(11):1010-1012.
[14] HaoY , QiuQY , WJ.Effeofa stragalu spoly saccharin (APS) only mphocyte- endothelim adhesion and themolecu-larme chanism[J].Immunnol J,2000, 16(3):206-209.
[15]尚德俊,王嘉桔,张柏根.中西医结合周围血管疾病学[M],北京:人民卫生出版社,2004,第1版:521-522.
[16]尚德俊,侯玉芬,陈柏楠.周围静脉疾病学[M],北京:人民军医出版社,2001,第1版:28-29.
[17]池明宇.中西医结合血栓病学[M],北京:人民卫生出版社,2004,第1版:445.
[18]施新猷.现代医学实验动物学[M],北京:人民军医出版社,2000,第1版:332-335.
[19] Reyers I,Mussoni L,Donati MB,et al.Failure of aspirin at different doses to modify experimental thrombosis in rats[J].Thromb Res,1980;18(5):669-674.
[20] Cho JS,Martelli E,Mozes G,et al.Effects of thrombolysis and venous thrombectomy on valvular compelence,thrombogenicity,venous wall morphology and function[J].J Vasc Surg,1998;28(5):787-799.
[21]李萍.奚九一教授治疗血栓性深静脉炎的经验介绍[J].贵阳中医学院学报,1999;21(1):14-16.
[22]杨博华,陈蕾,贺晓芳.行气活血清热利湿法治疗下肢深静脉血栓形成[J].中国中西医结合外科杂志,2003;9(2):99-100.
[23]朱之升,陈碧岚.中西医结合治疗髋部术后静脉血栓形成[J].浙江中西医结合杂志,2004;14(5):298-299.
[24]张莉莉.杜家经治疗下肢深部静脉血栓形成经验[J].湖南中医杂志,1999,15(4):20.
[25]岳端亭,王东.自拟消栓1号方治疗深静脉血栓46例[J].安徽中医临床杂志,2003,15(6):475.
[26] Dahlback B.Inherited Thrombophilia:resistance to activated protein Cas a pathogenic factor of venous thromboembolism[J].Blood,1985;85:607.
[27] Dahlbaek B,Hildebrand B.Inherited resistance to activated protein C is corrected by anticoagulant cofactor activity found to be a poperty of factor V[J].proc Natl AcadSci USA,1994,9l(2):1396.
[28] Bertina RM,Koeleman BP,Koster T.Mutation in blood coagulationfactor V associated with resisance to activated protein C[J].Nature,1994,369(6475):64.
[29] Voorbeg J,Roclse J,Koopman R,et a1.Association of idiopathic throm- boembolism with single point-mutation at Agr 506 of factor V[J].Lancet,1994,343(10):1535.
[30]王钦红.抗活化蛋白C是引起静脉血栓形成的一个重要原因[J].中华血液学杂志,1996,(9):499.
[31]储海燕,诸江,王鸿利,等.上海地区深静脉血栓形成患者抗活化蛋白C及FV Leiden突变的初步调查[J].中华血液学杂志,1996,(9):462
[32] Thomas DP,Merton RE,Wood RD,et al.The relationship between vessel wall injury and venous thrombosis:an experimential study[J].Br Haematol 1985,59(3):449.
[33] Carter Cb,Anderson FA,Wheeler HB:Epidemiology and patholphysiology of Venous thromboembolism.In Hull RD,Raskob GE,Pineo GF(eds):VenousThrom -bolism:An Evidence-based Atlas[M].Armonk,NY,Futura Publishing Company, 19963.
[34] Luscher TB,Barton M.Biology of the endothelium[J].Clin Cardiol,1997,20(suppl I):II3-10.
[35] Celermajer DS.Endothelial dysfunction:Do it matters?Is it reversible?[J] J Am Cardiol 1997,30(2):325-333.
[36] Hunt BJ , Jurd KM.Endothelial cell activation : a central pathophysiologica process[J].B M J,1998,316(7141):1328-1329.
[37] Tilley R,Mackman N.Tissue factor in hemostasis and thrombosis.Semin[J] Thromb Hemost.2006;32(1):5-10.
[38] Polgar J,Matuskova J,Wagner DD.The P-selectin,tissue factor,coagulation triad[J].Thromb Haemost.2005;3(8):1590-1596.
[39] Del Conde I,Shrimpton CN,Thiagarajan P,et al.Tissue-factor-bearing microves-icles arise from lipid rafts and fuse with activated platelets to initiate coagulation[J].Blood.2005;106(5):1604-1611.
[40] Steffel J,Luscher TF,Tanner FC.Tissue factor in cardiovascular diseases: molecular mechanisms and clinical implications[J]. Circulation. 2006; 113(5):722-731.
[41] Mackman N.Regulation of the tissue factor gene[J].Thromb.Haemost.1997; 78(1):747-754.
[42] Key NS,Bach RR.Tissue factor as a therapeutic target[J].Thromb Haemost. 2001; 85(3):375-376.
[43] Morrissey JH.Tissue factor:in at the start…and the finish?[J].Thromb.Haemost. 2003;1(12):878-880.
[44] Ghosh S,May MJ,Kopp EB.NF-κB and Rel proteins:evolutionarily conserved mediators of immune responses[J].Annu.Rev.Immunol.1998;16:225-260.
[45] Li Q,Verma IM.NF-κB regulation in the immune system[J].Nat.Rev.Immunol. 2002;10:725-730.
[46] Albert S,Baldwin Jr.The transcriptional factor NF-κB and human disease. [J]Clin. Invest.2001;107(12):3-6.
[47] Wakefield TW,Henke PK.The role of inflammation in early and late venous thrombosis:Are there clinical implications? [J]. Semin Vasc Surg. 2005; 18(2): 118-129.
[48] Viles-Gonzalez JF,Fuster V,Badimon JJ.Thrombin/inflammation paradigms: acloser look at arterial and venous thrombosis[J].Am.Heart.2005;149:(1 Suppl),19-31.
[49] Wakefield TW,Strieter RM.,Prince MR,et al.Pathogenesis of venous thrombosis:a new insight[J].Cardiovasc.Surg.1997;5(1):6-15.
[50] Springer TA.Traffic signals for lymphocyte recirculation and leukocyte emigration:the multistep paradigm[J].Cell.1994;76(2):301-314.
[51] Laudanna C,Kim JY,Constantin G,et al.Rapid leukocyte integrin activation by chemokines[J].Immunol Rev.2002;186:37-46.
[52] Furie B,Furie BC,Flaumenhaft RA.A journey with platelet P-selectin:the molecular basis of granule secretion,signalling and cell adhesion[J].Thromb.Haemost.2001; 86(1):214-221.
[53] McEver RP.Selectins:lectins that initiate cell adhesion under flow[J]. Curr.Opin.Cell Biol.2002;14(5):581-586.
[54] Geng JG,Chen M,Chou KC.P-selectin cell adhesion molecule in inflammation,thrombosis , cancer growth andmetastasis[J]. Curr.Med. Chem.2004 ; 11 : 2153-2160.
[55] Ma YQ,Plow EF,Geng JG.P-selectin binding to P-selectin glycoprotein ligand-1 induces an intermediate state ofαM 2 activation and acts cooperatively with extracellular stimuli to support maximal adhesion of human neutrophils[J].Blood. 2004;104(8):2549-2556.
[56] Atarashi K,Hirata T,Matsumoto M,et al.Rolling of Th1 cells via P-selectin glycoprotein ligand-1 stimulates LFA-1-mediated cell binding to ICAM-1[J]. Immunol.2005;174(3):1424-1432.
[57] Woollard KJ,Kling D,Kulkarni S,et al.Raised plasma soluble P-selectin in peripheral arterial occlusive disease enhances leukocyte adhesion [J].Circ.Res. 2006; 98(1):149-156.
[58] Hamyd AG,Wolf H,Albrecht S.Defective function of peripheral blood monocytes from patients with non-Hodgkin’s lymphoma [J]. Turk. J. Haemato.200118(2): 173-178.
[59] Blann AD, Noteboom WM,Rosendaal FR. Increased soluble P-selectin levels following deep venous thrombosis, cause or effect?Br J Haematol,2000, 108(1):191-193.
[60] Polanowska-Grabowska R,Gibbins JM.Gear AR. Plateletadhesion to collagen and collagen-related peptide under flow:rolesof the a2(3t integrin, GP VI,and src tyrosine kinases. ArteriosclerThromb Vasc Biol,2003, 23(10):1934-1940.
[61] Siljander PR, Munnix IC, Smethurst PA, et al. Platelet receptor- interplay regulates collagen-induced thrombus formation inflowing human blood. Blood. 2004,103(4):1333-1347.
[62] Yang LC, Wang CJ. Lee TH, et al. Early diagnosis of deep vein thrombosis in female patients who undergo total knee arthroplasty with measurement of P-se[ectin activation, f Vasc Surg, 2002, 35(4):702-712.
[63] LoPresti R, Ferrara F, Canino B, et al. Deep venous thrombosis: Leukocyte rheology at baseline and after in vitro activation.Haemostasis, 2000,30(4):168-173.
[64] Caimi G, Ganino B, Ferrara F, et al. Leukocyte rheology beforeand after chemotactic activation in some venous disease. Eur f Vasc Endovasc Surg, 1999, 18(5);411-416.
[65] Mine S, Tanaka Y, 5uematn M, et al. Hepatocyte growth factoris a potent trigger of neutrophil adhesion through rapid activationof lymphocyte function-associated antigen-1.[J] Lab Invest, 1998,78(11):1395-1404.
[66] Henke PK, DeBrunye 1.A, Sirieter RM,et al. Viral IL.-10genetrans Ferdecreases infiammationand cell adhesion moleculeexpression in a rat model of venous thrombosis.[J] Immunol 2000,164(4):2131-2141.
[67] EvangelistaV,Manarini S,Rotondo S. et al. Platelet/ polymorp- honuclear Leukocyte interaction in dynamic conditions;evidence of adhesion cascade and cross talk between P-selectin and the beta2 integrin CDllb/CD18.[J] Blood1996. 88 (11):4183-4194.
[68] Goel MS,DiamondSI,.Neutrophil cathepsin G promotesprothrombinase and fibrin formation under flow conditions byactivating fibrinogen- adher- ent platelets. [J ]Biol Chem . 2003. 278(11):9458-9463.
[69] EvangelisV,Manarini S.CollerBS,etal.Roleof P-selectin. beta2- integ- rins,and Src tyrosine kinases in mouse neutrophil-platelet adhesion.[J].Thromb Haemost,2003.1(50):1048-1054.
[70]刘政,侯玉芬,周涛.深静脉血栓形成动物模型的建立及应用进展[J].中国中西医结合外科杂志,2005;11(5):451-453.
[71] Solis MM,Vitti M,Cook J,et al.Recombinant soluble human thrombomodulin a randomized,blinded assessment of prevention of venous thrombosis and effects on hemostatic parameters in a rat model[J].Thromb Res,1994;73(6):385-394.
[72] Stanton C,Ross RP,Hutson S,et al.Processing and expression of rat and human clotting factor-X-encoding cDNAs[J].Gene,1996;169(2):269-273.
[73]李仪奎,姜名瑛.中药药理学[M].北京:中国中医药出版社,1992,48-144.
[74]王振义,李家增,阮长耿.血栓与止血—基础理论与临床[M].第二版.上海:上海科学技术出版社,1996,374-385.
[75]黄雪柏.水蛭的实验和临床研究概况[J].湖南中医学院学报,1997,(1):74.
[76]黄国才,等.小檗碱对兔血小板TXA2和血浆中PGI2生成的影响[J].中国药理学报,1991,(6):526.
[77]李中原,涂秀华.红花黄色素的药理研究进展[J].中药新药与临床药理,2005,16(2):153.
[78] R,Dustin ML,Marlin SD,et al.a human intercellular adhesion molecule (ICAM-1) distinct from LFA-1 [J]. Immunol,1986,Aug 15;137(4):1270.
[79] Jobinc,Hellerbrand C,Licatoll,et al.Mediation by NF-KappaB of cytokine induced expression of intercellular adhesion molecule 1 in an intestinal epithelial cell line,a process blocked by proteasome inhibitors[J]. Gut,1998,Jun,42(6):779.
[80] Roebuck KA,Finnegan A.Regulation of intercellular adhesion molecule- 1(CD54) gene expression. [J]. Leukoc Biol.1999 Dec;66(6):876.
[81] Wissink S,Van de stolpe A,Caldenhoven E, et al.NF-kappaB/Rel family members regulating the ICAM-1,promoter in monocytic THP-1 cells[J]. Immunobiology,1997,Dec;198(1-3):50-54.
[82] Osboml L,Hessionc,Tizard R, et al.Direct expression cloning of vascular cell adhesion molecule 1, a cytokine induced endothelial protein that binds to lymphocytes [J].Cell,1989 Dec,22;59(6):1203-11.
[83] Moore KL,Stults NL,Diaz S,etc.Identification of a specific glycoprotein ligand for P-selectin(CD62) on myeloid cells[J].Cell Biol.1992; 118(20: 445-456.
[84] Sako D,Chang XJ,Barone KM,etc.Expression cloning of a functional glyco- protein ligand for P-selectin[J].Cell.1993;75(6):1179-1186.
[85]龙勉.选择子/配体相互作用的二维反应动力学[J].生物力学最新进展.北京.高等教育出版社,2001:17-25.
[86] Moore KL. Structure and function of P-selectin glycoprotein ligand- 1[J].Leuk lymphoma. 1998,29(10):1-15.
[87] McEver RP and Cummings RD. Role of PSGL-1 binding to selectins in leukocyte recruitment[J]. Clin. Invest.1997,100(3):485-492.
[88] Muthing J, Spanbroek R, Peter-Katalinic J,etc. Isolationand structural characterization of fucosylated gangliosides with line- arpoly-N-acetyllactosaminy- lchains from human granulocytes[J]. Glyco- biology 1996;6(2): 147-156.
[89] Park EY, Smith MJ, Stropp ES, Snapp KR, etc.Comparison of PSGL-1 microbead and neutrophil rolling: microvillus elongation stabilizesP- selectin bond clusters. Biophys[J]. 2002;82(4):1835-1847.
[90] Bruehl RE, Moore KL, Lorant DE, etc.Leukocyte activation induces surface redistribution of P-selectin glycoprotein ligand-1[J]. Leukocyte Biol.1997;61(4):489-499.
[91] Alonso-Lebrero JL, Serrador JM, Dominguez-Jimenez C,etc. Polari- zation andinteraction of adhesion molecules P-selectin glycoprotein ligand 1 and intercellular adhesion molecule 3 with moesin and ezrin in myeloid cells[J].Blood 2000;95(7):2413-2419.
[92] Walcheck B, Moore KL, McEver RP. Neutrophil-neutrophil interactions under hydrodynamic shear stress involve L-selectin and PSGL-1:a mechanism that amplifies initialleukocyte accumulation of P-selectin in vitro f Clin[J].Invest.1996; 98(2):1081-1087.
[93] Norman KE,Katopodis AG,Thoma G,etc.P-selectin glycoprotein ligang-1 supports rolling on E- and P-selectin in vivo[J].Blood. 2000;96(10): 3585-91.
[94] Xia L,Sperandio M,Yago T,etc.P-selectin glycoproteinligand-1deficient Mice Have impaired leukocyte tethering to E-selectin under flow[J]. ClinInvest.2002; 109(7):939-950.
[95] Hirata T,Furie BC,Fuire B.P-,E-,L-slectin mediate migration of activated CD8+ T lymphocytes into inflamed skin[J] Immunol.2002;169(80:4307-13.
[96] Sperandio M , Smith ML , Forlow SB , etc.P-selectin glycoprotein ligand-1 mediatesL-selectin-dependentleukocyterollinginvenules[J].Exp.Med.2003;197(10):1355-1363.
[97] Hicks AE,Nolan SL,Ridger VC.Recombiant P-selectin glycoprotein ligand-1 directly inhibits leukocyte rolling by all 3 selectins in vivo:complete inhibition of rolling is not required for anti-inflammatory effect[J].Blood.2003;101(8):3249-3256.
[1] Lindblad B,Sternby NH,Bergqvist D.Incidence of venous thromboembolism verified by necrospy over 30 years[J].BMJ,1991;302(6778):709-711.
[2] Collins LM.DeepVenousThrombosis[J].Nurse Pract Forum,1998;(3):163-169.
[3] Roumen Klappe EM,Den Heijer M,Van Uum SH,et al.Inflammatory response in the acute phase of deep vein thrombosis[J].J Vasc Surg,2002;35(4):701-706.
[4] Eftychiou V.Clinical diagnosis and management of the patient with deep venous thromboembolism and acute pulmonary embolism[J].Nurse Pract,1996;21(3):50-62.
[5] Fowkes FJI,Price JF,Fowkes FGR.Incidence of diagnosed deep vein thrombosis in the general population:systematic review[J].Eur J Vasc Endovasc Surg 2003;25:1–5.
[6] Kahn SR.The clinical diagnosis of deep venous thrombosis:integrating incidence, risk factors,and symptoms and signs[J].Arch Intern Med,1998;158(21):2315–2323.
[7] Kakkar VV,Lawrence D.Hemodynamic and clinical assessment after therapy for acute deep vein thrombosis.A prospective study[J].Am J Surg,1985;15(4A):54-63.
[8] Coon WW.Venous thromboembolism.Prevalence,risk factors,and prevention[J].Clin Chest Med,1984;5(3):391-401.
[9] Viles-Gonzalez JF,Fuster V,Badimon JJ.Thrombin/inflammation paradigms:acloser look at arterial and venous thrombosis[J].Am.Heart.2005;149:(1 Suppl),19-31.
[10] Wakefield TW,Strieter RM.,Prince MR,et al.Pathogenesis of venous thrombosis:a new insight[J].Cardiovasc.Surg.1997;5:6-15.
[11] Springer TA.Traffic signals for lymphocyte recirculation and leukocyte emigration:the multistep paradigm[J].Cell.1994;76:301-314.
[12] Laudanna C,Kim JY,Constantin G,et al.Rapid leukocyte integrin activation by chemokines[J].Immunol Rev.2002;186:37-46.
[13] Furie B,Furie BC,Flaumenhaft RA.A journey with platelet P-selectin:the molecular basis of granule secretion , signalling and cell adhesion [J].Thro -mb.Haemost.2001;86:214-221.
[14] McEver RP.Selectins:lectins that initiate cell adhesion under flow[J].Curr.Opin.Cell Biol.2002;14:581-586.
[15] Geng JG,Chen M,Chou KC.P-selectin cell adhesion molecule in inflammation,thrombosis,cancer growth and metastasis[J].Curr.Med. Chem.2004;11:2153-2160.
[16] Ma YQ,Plow EF,Geng JG.P-selectin binding to P-selectin glycoprotein ligand-1 induces an intermediate state ofαM 2 activation and acts cooperatively with extracellular stimuli to support maximal adhesion of human neutrophils [J].Blood. 2004;104:2549-2556.
[17] Atarashi K,Hirata T,Matsumoto M,et al.Rolling of Th1 cells via P-selectin glycoprotein ligand-1 stimulates LFA-1-mediated cell binding to ICAM-1 [J]. Immunol.2005;174:1424-1432.
[18] Woollard KJ,Kling D,Kulkarni S,et al.Raised plasma soluble P-selectin in peripheral arterial occlusive disease enhances leukocyte adhesion[J].Circ.Res. 2006;98:149-156.
[19] Hamyd AG,Wolf H,Albrecht S.Defective function of peripheral blood monocytes from patients with non-Hodgkin’s lymphoma[J]. Turk.J. Haemato.2001;18:173-178.
[20] Bucek RA,Reiter M.Quehenberger P, et al, The role of solublecell adhesion molecules in patients with suspected deep venousthrombosis. Blood Coagul Fibrinolysis, 2003,14(7):653-657.
[21] Blann AD, Noteboom WM,Rosendaal FR. Increased soluble P-selectin levels following deep venous thrombosis, cause or effect?Br J Haematol,2000, 108(1):191-193.
[22] Polanowska-Grabowska R,Gibbins JM.Gear AR. Plateletadhesion to collagen and collagen-related peptide under flow:rolesof the a2(3t integrin, GP VI,and src tyrosine kinases. ArteriosclerThromb Vasc Biol,2003, 23(10):1934-1940.
[23] Siljander PR, Munnix IC, Smethurst PA, et al. Platelet recepto- rinterplay regulates collagen-induced thrombus formation inflowing human blood. Blood. 2004,103(4):1333-1347.
[24] Yang LC, Wang CJ. Lee TH, et al. Early diagnosis of deep vein thrombosis in female patients who undergo total knee arthroplasty with measurement of P-se[ectin activation, f Vasc Surg, 2002, 35(4):702-712
[25] LoPresti R, Ferrara F, Canino B, et al. Deep venous thrombosis: Leukocyte rheology at baseline and after in vitro activation.Haemostasis, 2000, 30(4):168-173.
[26] Caimi G,Ganino B, Ferrara F, et al. Leukocyte rheology beforeand after chemotactic activation in some venous disease.Eur f Vasc Endovasc Surg,1999,18(5);411-416
[27] Mine S, Tanaka Y, 5uematn M, et al. Hepatocyte growth factoris a potent trigger of neutrophil adhesion through rapid activationof lymphocyte function-associated antigen-1.[J] Lab Invest, 1998,78(11):1395-1404.
[28] Henke PK, DeBrunye 1.A, Sirieter RM,et al. Viral IL.-10genetrans Fer- decreases infiammationand cell adhesion moleculeexpression in a rat model of venous thrombosis.[J] Immunol 2000,164(4):2131-2141.
[29] EvangelistaV,Manarini S,Rotondo S. et al. Platelet/ polymor- phonuclear Leukocyte interaction in dynamic conditions;evidence of adhesion cascade and cross talk between P-selectin and the beta2 integrin CDllb/CD18.[J] Blood1996. 88 (.11):4183-4194.
[30] Goel MS,DiamondSI,.Neutrophil cathepsin G promotesprothrombinase and fibrin formation under flow conditions byactivating fibrinogen- adherent platelets. [J]Biol Chem . 2003. 278(11):9458-9463.
[31] EvangelisV,Manarini S.CollerBS,etal.Roleof P-selectin. beta2- inte- grins,and Src tyrosine kinases in mouse neutrophil-platelet adhesion. [J]Thromb Haemost, 2003. 1(50):1048-1054
[32] Thanaporn P , MyersDD. Wrobleski SK , etal.P-selectininhibition decreases post-thrombotic vein wall fibrosis in a ratmodel. Surgery, 2003,134(2);365-371.
[33] Myers DD,Jr,Henke K ,Wrobleski SK,et al. P-selectin inhibition enhances thrombus resolution and decreases vein wall fibrosis in a rat model. [J]Vasc Surg,2002,36(5):928-938.
[34] Simon DI,Chen I, Xu H, et al. Platelet glycoprotein ibalpha is a counter receptor the leukocyte integrin Mac-1 (CD116/CD18).[J] Exp Med,2000,192(2):193-204.
[35] Wang JS,LiaoCH. Moderate-intensity exercise suppresses platelet activation and poly morphonuclear leukocyte interaction with surface- adherent platelet under shear flow in men. Thromb Haemost,2004. 91(3):587-594.
[1] Nishibori M,Takahashi HK,Mori S.The regulation of ICAM-1 and LFA-1 interaction by autacoids and statins:a novel strategy for controlling inflammation and immune reponses[J].J Pharmacol Sci.2003;92(1):7-12.
[2] WuY,ZhuBD.Effect of DangguiBuxue Decoctiononpro-liferation and expression of interce-llular adhesion molecule-1inhumanumbilicalvein endothelialcells[J].J West China UnivMedSci,2001,32(4):593-595.
[3] ZhangYJ,ZhaoLG,WuXZ.Effect of HuoxuehuayuDe–coctionon expression of adhesivemolecularofintrapulmonicendothelialcellofratssufferedfromSAP[J].ChinTraditHerbDrugs,2001,32(11):1010-1012.
[4] HaoY,QiuQY,WJ. Effect of astragalus poly saccharin(APS) only Mphocyte -endothelium adhesion and th molecu–larmechanism [J]. ImmunnolJ, 2000, 16(3): 206-20.
[5] Ross R.The pathogenesis of atherosclerosis:a perspective for the 1990s[J].Nature 1993; 62(29):801.
[6] Rosenson Rs,Tangeney CC.Antiathero thrombotic properties of stains:implications for cardiovascular event reduction [J].JAMA 1998;279:1643-50.
[7] Peterk,WeirichU,NordtTK,etal.Solublevascular cell adhesion molecule-1(VCAM-1) as potential marker of atherosclerosis[J].Thromb Haemost. 1999;82 Suppl 38-43.
[8] Prksh,Park JH,Kang JS,etal.Involvement of transcription factor sinplasma HDL Protection against TNF-a lpha-induced vascular cell adhesion molecule- 1expression [J].IntJBiochemCellBiol,2003,35(2):168-182.
[9] Codkerill BW, Huehnsty, Weerasinghea, etal. Elevation of plasmahigh-density Lipoprotein concentration reduce sinterleukin-1-induced expression of E-selectin in Aninvivomodel of acutein flammation[J].Circulation,2001,103(1):108-112.
[10] Dmayugap,ZhuJ,Oguchis,etal.ReconstitutedHDLcontaininghuman apolipoprotein A-Ireduces VCAM-1 expression andneointima formation following peria dventitial cuff-induced carotid injury in a poenull mice[J]. Biochem Biophys Res Commun, 1999,264(2):465-468.
[11] CleeM,KasteleinJJ,VandaMM,etal.Ageand residualcholesteroleffluxaffect HDL cholesterollevelsandcoronary artery disease in ABCA1 heterozygotes [J]. J Clin Invest,2000,106(10):1263-1270.
[12] ConnellBJ,GenestJJr.High-density lipoproteins and endothelial function [J]. Circu- lation, 2001,104(16):1978-1983.
[13] ContiCR.Updatedpathophysiologic concept sinunstable coro-nary artery disease [J]. AmHeartJ,2001,141:12-14.
[14] RusHG,VlaicuR,NiculescuF.Interleukin-6 and interleukin-8 protein and gene in human arteriol atherosclerotic wall[J].Atherosclerosis,1996,127:263-271.
[15] SugiyamaS,OkadaY,SukhovaGK,etal.Macropha gemyeloperoxidase regulation by granulocyte macrophagecolony stimulating factor in human atherosclerosis and implication sina-cutecoronary syndromes[J].AmJPathol,2001,158:879-891.
[16] SimoniniA,MoscucciM,MullerDWM,etal.IL-8 is a nangiogenic factor in human coronary atherectomy tissue[J].Circulation,2000,101:1519-1526.
[17] SarenP,WelgusHG,KovanenPT.TNF-a and IL-1 selective lyinduce expression of 92-k Dagelatinase by human macrophages[J].J Immunol,1996,157:4159-4165.
[18]陈利国,屈援,葛红颖,等.补阳还五汤对血瘀证大鼠血管内皮细胞黏附分子表达的影响[J].中草药,2005,36(5):706-708.
[19]王宗仁,李军昌,马爱玲,等.芪丹通脉片对动脉粥样硬化大鼠单个核细胞中细胞间黏附分子1及血管细胞黏附分子1 mRNA表达的影响[J].中国临床康复,2005,9(27):77-9.
[20]龙铟,刘莉,王宗仁,等.中药芪丹通脉片对心肌损伤大鼠血小板功能的影响[J].第四军医大学学报,2003,24(5):406-8.
[21]行利,马静,王宗仁,等.芪丹通脉片对大鼠急性心肌缺血损伤的影响[J].第四军医大学学报,2003,24(5):415-7.
[22]张路,吴宗贵.通心络对实验性家兔主动脉粥样斑块CAM-1表达影响的实验研究[J].中西医结合心脑血管病杂志,2003,1(12):705-706.
[23]陈建宗,田季雨,顾宜,等.复方丹参滴丸对动脉粥样硬化家兔颈动脉血管壁血管细胞黏附分子-1表达的影响[J].中国临床康复,2004,8(24):5048-9.
[24]刘春华,钱冠清,刘会齐,等.银杏叶提取物抑制轻度修饰低密度脂蛋白诱导的血管内皮细胞与单核细胞黏附的实验研究[J].中国中西医结合杂志,2000,20(12):917-9.
[25]赵桂峰,张红霞,范英昌.救心胶囊对损伤内皮细胞黏附因子表达的影响[J].天津中医药,2004,21(2):148-150.
[26]王宗仁,肖铁卉,李晶华,等.芪丹通脉片对肿瘤坏死因子-α诱导的心肌细胞的细胞间黏附分子-1表达的影响[J].中草药,2003,34(11):1035-6.
[27]苗榕生,张晓明,王红彦.醒脑静对急性脑梗塞患者细胞黏附分子及T细胞亚群的影响[J].北京中医药大学学报,2001,24(1):64-71.
[28]陈春富,贾海燕,曹霞,等.黄芪注射液对脑梗死患者外周血细胞黏附分子表达水平的影响[J].解放军医学杂志,2003,28(11):1048-9.
[29]陈根成,胡金城,朱成全,等.益气活血片对脑梗塞大鼠血小板膜黏附分子表达的影响[J].广州中医药大学学报,2003,20(1):48-50.
[30]胡跃强,胡国恒,吴云虎,等.清热化瘀颗粒治疗急性缺血性中风的临床研究[J].山东中医药大学学报,2004,28(1):31-3.
[31]刘萍,章怡祎,张静生.中药复方对损伤人血管内皮细胞表达细胞间黏附分子的影响[J].中国临床康复,2006,10(27):54-6.
[32]刘萍,张静生,郑菲,等.中药对低密度脂蛋白受体基因表达的影响[J].中国中西医结合急救杂志,2000,7(3):141-3.
[33]李树青,刘学英,贺宏.黄芪对冠心病心绞痛的防治作用中国中西医结合急救杂志[J].2002,9(5):270-2.
[34]雷燕,高倩,李悦山,等.黄芪、当归及其组方促血管内皮细胞增殖作用的研究中国中西医结合杂志[J].2002,4(1):21-2.
[35]吴勇,欧阳静萍,涂淑珍,等..黄芪多糖对动脉粥样硬化内皮细胞损伤的影响[J].湖北中医学院学报,2001,13(2):101-3.
[36]姜开余,顾振论,阮长耿.丹参素对CD116、P-selectin、ICAM-1,VCAM-1,E-selectin:表达的影响[J]中国药理学通报,2000,16(6):682.
[37] Chen Y H,Lin S J,Ku H H, et a1.Salvianolic acid Rattenuates VCAM-1 and ICAM-1 expression in TNF-αI-pha-treated huaman aortic endothelial cells.[J]J c cell Biochem, 2001, 82 (3):512
[38]曾素耘,樊素璇,蒋小青.川芎嗪对妊娠高血压综合征患者脐静脉内皮细胞黏附分子表达的抑制作用[J].中华妇产科杂志,2000,35(5):282.
[39]李敏杰,刘勇,马琳,等.葛根素对内皮细胞增殖及黏附分子表达的影响[J].陕西中医,2002,23(2):148.
[40]严群超,莫木顺,甘绍乃,等.葛根素对急性冠脉综合征患者血清可溶性黏附分子的影响[J].辽宁中医杂志,2002,29(6):340.
[41]何玉萍,陈奕芝,方若鸣,等.石菖蒲加冰片对高血脂大鼠血小板活化功能的影响[J].中国中医药科技,2003;10(6):337-8.
[42]沈晓君,魏群.通脉降脂口服液对动脉粥样硬化患者细胞黏附分子表达的影响[J].山东中医杂志,2004,23(10):584-5.
[43]张宇辉,刘国仗.黏附分子和黏附蛋白在冠心病发生发展中的作用[J].心血管病学进展,2000,21(2):113-5.
[44]李兰芳,张建新,兰漫野,等.通脉活血灵胶囊对实验性高脂血症家兔血脂及动脉粥样硬化的影响[J].中草药,2000,31(6):440-2.
[45]李越华,刘宇,顾仁樾.三七有效组分Rx对兔动脉粥样硬化的实验研究[J].中西医结合心脑血管病杂志,2003,1(10):582-4.
[46]孟振行,吴淑敏,孙仁俊,等.丹参防治动脉粥样硬化的机制[J].心脑血管病杂志,1993,12(1):121-3.
[47]周小明,陆再英,汪道文.丹参防治实验性动脉再狭窄及其机制的初步研究[J].中国中西医结合杂志,1996,16(8):480-2.
[48] Bucek RA,ReiterM.Quehenberger P, et al, The role of soluble cell adhesion molecules in patients with suspected deep venous thrombosis[J]. Blood Coagul Fibrinolysis, 2003,14(7):653-7.
[49] Blann AP, Noteboom WM, Rosendaal FR. Increased soluble P-selectin levels following deep venous thrombosis: cause or effect? [J]. Br J Haematol,2000, I08(1):191-3.
[50] LoPresti R, Ferrara F, Canino B, et al. Deep venous thrombosis Leukocyte theology at baseline and after in vitro activation[J].Haemostasis, 2000, 30(4): 168-173.
[51] Caimi G, Gianino B, Ferrara F, et al. Leukocyte theology before and after chemo- tactic activation in some venous disease. [J]. Eur J VasC Endovasc Surg, 1999, 18(5);411-6.
[52] Mine S, Tanaka Y, Suematn M, et al. Hepatocyte growth factor is a potent trigger of neutrophil adhesion through rapid activation of lymphocyte function-associated antigen-1[J]. L.ab Invest, 1998,78(11):1395-1404.
[53] Eppihimer MJ, Schaub RG. P-selectin-dependent inhibition of thrombosis during venous stasis[J]. Arterioscler Thromb Vasc Biol.2000,20( 11):2483-8.
[54] Henke PK, DeBrunye LA, Strietcr RM,et al. Viral IL.-10 genetransfer decreases inflammation and cell adhesion moleculeexpression in a rat model of venous thrombosis[J].JImmunol.2000,164(4):2131-2141.
[55] Konstantopoulos K, Neelamegham S, Burns AR, et al. Venouslevels of shear support neutrophil-platelet adhesion and neutrophilaggregation in blood via P-selectin and bata2-integrin[J].Circulation, 1998, 98(9):873-882.
[56] EvangelistsV,Manarini S, Rotondo S, et al.Platelet/polymorphonuclear leukocyte interaction in dynamic conditions;evidence of adhesion cascade and cross talk between P-selectin andthe beta2 integrin CDllb/CD18[J]. Blood. 1996. 88 (11): 4183-4194
[57] Goel MS,Diamond SI.Neutrophil cathepsin G promotesprothrombinase and fibrin formation under flow conditions by activating fibrinogen-adherent platelets[J]. J Biol C hem.2003.278(11):9458-9463.
[58] Evangelista V,Manarini S. Coller BS, et al.Role of P-selectinbeta2-integrinsand Sre tyrosine kinases in mouse neutrophil platelet adhesion[J]. J Thromh Haemost,2003.1(50):1048 -1054.
[59] Simon DI, Chen I, Xu H, et al. Platelet glycoprotein ibalpha is acounter receptor the leukocyte integrin Mac-1 (CD11b/CD18) [J]. JExp Med。2000, 192(2):193-204.
[60] Babinska A, Kedees MH, Athar H, et al. F11-receptor(F11F/JAM)mediates platelet adhesion to endothelial cells; role ininflammatory thrombosis[J]. Thromb Haemost,2002, 88(5):847-850
[61] Wakefield TW,Strieter RM,Downing LJ,et al. P-selectin andTNF inhibition reduce venous thrombosis inflammation[J]. J SurgRes. 1996, 64(1);26-31.
[62] Myers DD Jr, Hawley AE, Farris DM, et al. Cellular IL-10 ismore effective than viral IL-10 in decreasing venous thrombosis[J].JSurg Res. 2003, 112(2):168-174.
[63]王健,奚九一,张柏根.清营Ⅰ号对深静脉血栓形成形态学演变的实验研究[J].中国中西医结合外科杂志,2003,9(2):116-118.
[2] Collins LM.DeepVenousThrombosis[J].Nurse Pract Forum,1998(3):163-169.
[3] Roumen Klappe EM,Den Heijer M,Van Uum SH,et al.Inflammatory response in the acute phase of deep vein thrombosis[J].J Vasc Surg,2002;35(4):701-706.
[4] Eftychiou V.Clinical diagnosis and management of the patient with deep venous thromboembolism and acute pulmonary embolism[J].Nurse Pract,1996;21(3):50-62.
[5] Fowkes FJ,Price JF,Fowkes FG..Incidence of diagnosed deep vein thrombosis in the general population:systematic review[J].Eur J Vasc Endovasc Surg 2003;25(1):1–5.
[6] Kahn SR.The clinical diagnosis of deep venous thrombosis:integrating incidence, risk factors,and symptoms and signs[J].Arch Intern Med,1998;15(21):2315–2323.
[7] Kakkar VV,Lawrence D.Hemodynamic and clinical assessment after therapy for acute deep vein thrombosis.A prospective study[J].Am J Surg,1985;15(4A):54-63.
[8] Coon WW.Venous thromboembolism.Prevalence,risk factors,and prevention[J].Clin Chest Med,1984;5(3):391-401.
[9] Ross R.The pathogenesis of atherosclerosis:a perspective for the 1990s[J].Nature 1993;62(29):801.
[10] Rosenson Rs,Tangeney CC.Antiathero thrombotic properties of stains::implications for cardiovascular event reduction [J].JAMA 1998;279::1643-50.
[11] Peterk,Weirich U,NordtTK, etal.Soluble vascular cell adhesion molecule- 1(VCAM-1) as potential marker of atherosclerosis[J].Thromb Haemost. 1999;82 Suppl 38-43.
[12] WuY,ZhuBD.Effect of DangguiBuxue Decoctiononpro-liferation and expre- ssion of intercellular adhesion molecule-1 in human umbilicalvein endothelialcells[J]. West China Univ Med Sci,2001,32(4):593-595.
[13] ZhangYJ,ZhaoLG,WuXZ.Effect of HuoxuehuayuDe–coctionon expression of adhe-sive molecular of intrapulmon icendothelial cell of rat suffered fromSAP[J].China Tradit Herb Drugs,2001,32(11):1010-1012.
[14] HaoY , QiuQY , WJ.Effeofa stragalu spoly saccharin (APS) only mphocyte- endothelim adhesion and themolecu-larme chanism[J].Immunnol J,2000, 16(3):206-209.
[15]尚德俊,王嘉桔,张柏根.中西医结合周围血管疾病学[M],北京:人民卫生出版社,2004,第1版:521-522.
[16]尚德俊,侯玉芬,陈柏楠.周围静脉疾病学[M],北京:人民军医出版社,2001,第1版:28-29.
[17]池明宇.中西医结合血栓病学[M],北京:人民卫生出版社,2004,第1版:445.
[18]施新猷.现代医学实验动物学[M],北京:人民军医出版社,2000,第1版:332-335.
[19] Reyers I,Mussoni L,Donati MB,et al.Failure of aspirin at different doses to modify experimental thrombosis in rats[J].Thromb Res,1980;18(5):669-674.
[20] Cho JS,Martelli E,Mozes G,et al.Effects of thrombolysis and venous thrombectomy on valvular compelence,thrombogenicity,venous wall morphology and function[J].J Vasc Surg,1998;28(5):787-799.
[21]李萍.奚九一教授治疗血栓性深静脉炎的经验介绍[J].贵阳中医学院学报,1999;21(1):14-16.
[22]杨博华,陈蕾,贺晓芳.行气活血清热利湿法治疗下肢深静脉血栓形成[J].中国中西医结合外科杂志,2003;9(2):99-100.
[23]朱之升,陈碧岚.中西医结合治疗髋部术后静脉血栓形成[J].浙江中西医结合杂志,2004;14(5):298-299.
[24]张莉莉.杜家经治疗下肢深部静脉血栓形成经验[J].湖南中医杂志,1999,15(4):20.
[25]岳端亭,王东.自拟消栓1号方治疗深静脉血栓46例[J].安徽中医临床杂志,2003,15(6):475.
[26] Dahlback B.Inherited Thrombophilia:resistance to activated protein Cas a pathogenic factor of venous thromboembolism[J].Blood,1985;85:607.
[27] Dahlbaek B,Hildebrand B.Inherited resistance to activated protein C is corrected by anticoagulant cofactor activity found to be a poperty of factor V[J].proc Natl AcadSci USA,1994,9l(2):1396.
[28] Bertina RM,Koeleman BP,Koster T.Mutation in blood coagulationfactor V associated with resisance to activated protein C[J].Nature,1994,369(6475):64.
[29] Voorbeg J,Roclse J,Koopman R,et a1.Association of idiopathic throm- boembolism with single point-mutation at Agr 506 of factor V[J].Lancet,1994,343(10):1535.
[30]王钦红.抗活化蛋白C是引起静脉血栓形成的一个重要原因[J].中华血液学杂志,1996,(9):499.
[31]储海燕,诸江,王鸿利,等.上海地区深静脉血栓形成患者抗活化蛋白C及FV Leiden突变的初步调查[J].中华血液学杂志,1996,(9):462
[32] Thomas DP,Merton RE,Wood RD,et al.The relationship between vessel wall injury and venous thrombosis:an experimential study[J].Br Haematol 1985,59(3):449.
[33] Carter Cb,Anderson FA,Wheeler HB:Epidemiology and patholphysiology of Venous thromboembolism.In Hull RD,Raskob GE,Pineo GF(eds):VenousThrom -bolism:An Evidence-based Atlas[M].Armonk,NY,Futura Publishing Company, 19963.
[34] Luscher TB,Barton M.Biology of the endothelium[J].Clin Cardiol,1997,20(suppl I):II3-10.
[35] Celermajer DS.Endothelial dysfunction:Do it matters?Is it reversible?[J] J Am Cardiol 1997,30(2):325-333.
[36] Hunt BJ , Jurd KM.Endothelial cell activation : a central pathophysiologica process[J].B M J,1998,316(7141):1328-1329.
[37] Tilley R,Mackman N.Tissue factor in hemostasis and thrombosis.Semin[J] Thromb Hemost.2006;32(1):5-10.
[38] Polgar J,Matuskova J,Wagner DD.The P-selectin,tissue factor,coagulation triad[J].Thromb Haemost.2005;3(8):1590-1596.
[39] Del Conde I,Shrimpton CN,Thiagarajan P,et al.Tissue-factor-bearing microves-icles arise from lipid rafts and fuse with activated platelets to initiate coagulation[J].Blood.2005;106(5):1604-1611.
[40] Steffel J,Luscher TF,Tanner FC.Tissue factor in cardiovascular diseases: molecular mechanisms and clinical implications[J]. Circulation. 2006; 113(5):722-731.
[41] Mackman N.Regulation of the tissue factor gene[J].Thromb.Haemost.1997; 78(1):747-754.
[42] Key NS,Bach RR.Tissue factor as a therapeutic target[J].Thromb Haemost. 2001; 85(3):375-376.
[43] Morrissey JH.Tissue factor:in at the start…and the finish?[J].Thromb.Haemost. 2003;1(12):878-880.
[44] Ghosh S,May MJ,Kopp EB.NF-κB and Rel proteins:evolutionarily conserved mediators of immune responses[J].Annu.Rev.Immunol.1998;16:225-260.
[45] Li Q,Verma IM.NF-κB regulation in the immune system[J].Nat.Rev.Immunol. 2002;10:725-730.
[46] Albert S,Baldwin Jr.The transcriptional factor NF-κB and human disease. [J]Clin. Invest.2001;107(12):3-6.
[47] Wakefield TW,Henke PK.The role of inflammation in early and late venous thrombosis:Are there clinical implications? [J]. Semin Vasc Surg. 2005; 18(2): 118-129.
[48] Viles-Gonzalez JF,Fuster V,Badimon JJ.Thrombin/inflammation paradigms: acloser look at arterial and venous thrombosis[J].Am.Heart.2005;149:(1 Suppl),19-31.
[49] Wakefield TW,Strieter RM.,Prince MR,et al.Pathogenesis of venous thrombosis:a new insight[J].Cardiovasc.Surg.1997;5(1):6-15.
[50] Springer TA.Traffic signals for lymphocyte recirculation and leukocyte emigration:the multistep paradigm[J].Cell.1994;76(2):301-314.
[51] Laudanna C,Kim JY,Constantin G,et al.Rapid leukocyte integrin activation by chemokines[J].Immunol Rev.2002;186:37-46.
[52] Furie B,Furie BC,Flaumenhaft RA.A journey with platelet P-selectin:the molecular basis of granule secretion,signalling and cell adhesion[J].Thromb.Haemost.2001; 86(1):214-221.
[53] McEver RP.Selectins:lectins that initiate cell adhesion under flow[J]. Curr.Opin.Cell Biol.2002;14(5):581-586.
[54] Geng JG,Chen M,Chou KC.P-selectin cell adhesion molecule in inflammation,thrombosis , cancer growth andmetastasis[J]. Curr.Med. Chem.2004 ; 11 : 2153-2160.
[55] Ma YQ,Plow EF,Geng JG.P-selectin binding to P-selectin glycoprotein ligand-1 induces an intermediate state ofαM 2 activation and acts cooperatively with extracellular stimuli to support maximal adhesion of human neutrophils[J].Blood. 2004;104(8):2549-2556.
[56] Atarashi K,Hirata T,Matsumoto M,et al.Rolling of Th1 cells via P-selectin glycoprotein ligand-1 stimulates LFA-1-mediated cell binding to ICAM-1[J]. Immunol.2005;174(3):1424-1432.
[57] Woollard KJ,Kling D,Kulkarni S,et al.Raised plasma soluble P-selectin in peripheral arterial occlusive disease enhances leukocyte adhesion [J].Circ.Res. 2006; 98(1):149-156.
[58] Hamyd AG,Wolf H,Albrecht S.Defective function of peripheral blood monocytes from patients with non-Hodgkin’s lymphoma [J]. Turk. J. Haemato.200118(2): 173-178.
[59] Blann AD, Noteboom WM,Rosendaal FR. Increased soluble P-selectin levels following deep venous thrombosis, cause or effect?Br J Haematol,2000, 108(1):191-193.
[60] Polanowska-Grabowska R,Gibbins JM.Gear AR. Plateletadhesion to collagen and collagen-related peptide under flow:rolesof the a2(3t integrin, GP VI,and src tyrosine kinases. ArteriosclerThromb Vasc Biol,2003, 23(10):1934-1940.
[61] Siljander PR, Munnix IC, Smethurst PA, et al. Platelet receptor- interplay regulates collagen-induced thrombus formation inflowing human blood. Blood. 2004,103(4):1333-1347.
[62] Yang LC, Wang CJ. Lee TH, et al. Early diagnosis of deep vein thrombosis in female patients who undergo total knee arthroplasty with measurement of P-se[ectin activation, f Vasc Surg, 2002, 35(4):702-712.
[63] LoPresti R, Ferrara F, Canino B, et al. Deep venous thrombosis: Leukocyte rheology at baseline and after in vitro activation.Haemostasis, 2000,30(4):168-173.
[64] Caimi G, Ganino B, Ferrara F, et al. Leukocyte rheology beforeand after chemotactic activation in some venous disease. Eur f Vasc Endovasc Surg, 1999, 18(5);411-416.
[65] Mine S, Tanaka Y, 5uematn M, et al. Hepatocyte growth factoris a potent trigger of neutrophil adhesion through rapid activationof lymphocyte function-associated antigen-1.[J] Lab Invest, 1998,78(11):1395-1404.
[66] Henke PK, DeBrunye 1.A, Sirieter RM,et al. Viral IL.-10genetrans Ferdecreases infiammationand cell adhesion moleculeexpression in a rat model of venous thrombosis.[J] Immunol 2000,164(4):2131-2141.
[67] EvangelistaV,Manarini S,Rotondo S. et al. Platelet/ polymorp- honuclear Leukocyte interaction in dynamic conditions;evidence of adhesion cascade and cross talk between P-selectin and the beta2 integrin CDllb/CD18.[J] Blood1996. 88 (11):4183-4194.
[68] Goel MS,DiamondSI,.Neutrophil cathepsin G promotesprothrombinase and fibrin formation under flow conditions byactivating fibrinogen- adher- ent platelets. [J ]Biol Chem . 2003. 278(11):9458-9463.
[69] EvangelisV,Manarini S.CollerBS,etal.Roleof P-selectin. beta2- integ- rins,and Src tyrosine kinases in mouse neutrophil-platelet adhesion.[J].Thromb Haemost,2003.1(50):1048-1054.
[70]刘政,侯玉芬,周涛.深静脉血栓形成动物模型的建立及应用进展[J].中国中西医结合外科杂志,2005;11(5):451-453.
[71] Solis MM,Vitti M,Cook J,et al.Recombinant soluble human thrombomodulin a randomized,blinded assessment of prevention of venous thrombosis and effects on hemostatic parameters in a rat model[J].Thromb Res,1994;73(6):385-394.
[72] Stanton C,Ross RP,Hutson S,et al.Processing and expression of rat and human clotting factor-X-encoding cDNAs[J].Gene,1996;169(2):269-273.
[73]李仪奎,姜名瑛.中药药理学[M].北京:中国中医药出版社,1992,48-144.
[74]王振义,李家增,阮长耿.血栓与止血—基础理论与临床[M].第二版.上海:上海科学技术出版社,1996,374-385.
[75]黄雪柏.水蛭的实验和临床研究概况[J].湖南中医学院学报,1997,(1):74.
[76]黄国才,等.小檗碱对兔血小板TXA2和血浆中PGI2生成的影响[J].中国药理学报,1991,(6):526.
[77]李中原,涂秀华.红花黄色素的药理研究进展[J].中药新药与临床药理,2005,16(2):153.
[78] R,Dustin ML,Marlin SD,et al.a human intercellular adhesion molecule (ICAM-1) distinct from LFA-1 [J]. Immunol,1986,Aug 15;137(4):1270.
[79] Jobinc,Hellerbrand C,Licatoll,et al.Mediation by NF-KappaB of cytokine induced expression of intercellular adhesion molecule 1 in an intestinal epithelial cell line,a process blocked by proteasome inhibitors[J]. Gut,1998,Jun,42(6):779.
[80] Roebuck KA,Finnegan A.Regulation of intercellular adhesion molecule- 1(CD54) gene expression. [J]. Leukoc Biol.1999 Dec;66(6):876.
[81] Wissink S,Van de stolpe A,Caldenhoven E, et al.NF-kappaB/Rel family members regulating the ICAM-1,promoter in monocytic THP-1 cells[J]. Immunobiology,1997,Dec;198(1-3):50-54.
[82] Osboml L,Hessionc,Tizard R, et al.Direct expression cloning of vascular cell adhesion molecule 1, a cytokine induced endothelial protein that binds to lymphocytes [J].Cell,1989 Dec,22;59(6):1203-11.
[83] Moore KL,Stults NL,Diaz S,etc.Identification of a specific glycoprotein ligand for P-selectin(CD62) on myeloid cells[J].Cell Biol.1992; 118(20: 445-456.
[84] Sako D,Chang XJ,Barone KM,etc.Expression cloning of a functional glyco- protein ligand for P-selectin[J].Cell.1993;75(6):1179-1186.
[85]龙勉.选择子/配体相互作用的二维反应动力学[J].生物力学最新进展.北京.高等教育出版社,2001:17-25.
[86] Moore KL. Structure and function of P-selectin glycoprotein ligand- 1[J].Leuk lymphoma. 1998,29(10):1-15.
[87] McEver RP and Cummings RD. Role of PSGL-1 binding to selectins in leukocyte recruitment[J]. Clin. Invest.1997,100(3):485-492.
[88] Muthing J, Spanbroek R, Peter-Katalinic J,etc. Isolationand structural characterization of fucosylated gangliosides with line- arpoly-N-acetyllactosaminy- lchains from human granulocytes[J]. Glyco- biology 1996;6(2): 147-156.
[89] Park EY, Smith MJ, Stropp ES, Snapp KR, etc.Comparison of PSGL-1 microbead and neutrophil rolling: microvillus elongation stabilizesP- selectin bond clusters. Biophys[J]. 2002;82(4):1835-1847.
[90] Bruehl RE, Moore KL, Lorant DE, etc.Leukocyte activation induces surface redistribution of P-selectin glycoprotein ligand-1[J]. Leukocyte Biol.1997;61(4):489-499.
[91] Alonso-Lebrero JL, Serrador JM, Dominguez-Jimenez C,etc. Polari- zation andinteraction of adhesion molecules P-selectin glycoprotein ligand 1 and intercellular adhesion molecule 3 with moesin and ezrin in myeloid cells[J].Blood 2000;95(7):2413-2419.
[92] Walcheck B, Moore KL, McEver RP. Neutrophil-neutrophil interactions under hydrodynamic shear stress involve L-selectin and PSGL-1:a mechanism that amplifies initialleukocyte accumulation of P-selectin in vitro f Clin[J].Invest.1996; 98(2):1081-1087.
[93] Norman KE,Katopodis AG,Thoma G,etc.P-selectin glycoprotein ligang-1 supports rolling on E- and P-selectin in vivo[J].Blood. 2000;96(10): 3585-91.
[94] Xia L,Sperandio M,Yago T,etc.P-selectin glycoproteinligand-1deficient Mice Have impaired leukocyte tethering to E-selectin under flow[J]. ClinInvest.2002; 109(7):939-950.
[95] Hirata T,Furie BC,Fuire B.P-,E-,L-slectin mediate migration of activated CD8+ T lymphocytes into inflamed skin[J] Immunol.2002;169(80:4307-13.
[96] Sperandio M , Smith ML , Forlow SB , etc.P-selectin glycoprotein ligand-1 mediatesL-selectin-dependentleukocyterollinginvenules[J].Exp.Med.2003;197(10):1355-1363.
[97] Hicks AE,Nolan SL,Ridger VC.Recombiant P-selectin glycoprotein ligand-1 directly inhibits leukocyte rolling by all 3 selectins in vivo:complete inhibition of rolling is not required for anti-inflammatory effect[J].Blood.2003;101(8):3249-3256.
[1] Lindblad B,Sternby NH,Bergqvist D.Incidence of venous thromboembolism verified by necrospy over 30 years[J].BMJ,1991;302(6778):709-711.
[2] Collins LM.DeepVenousThrombosis[J].Nurse Pract Forum,1998;(3):163-169.
[3] Roumen Klappe EM,Den Heijer M,Van Uum SH,et al.Inflammatory response in the acute phase of deep vein thrombosis[J].J Vasc Surg,2002;35(4):701-706.
[4] Eftychiou V.Clinical diagnosis and management of the patient with deep venous thromboembolism and acute pulmonary embolism[J].Nurse Pract,1996;21(3):50-62.
[5] Fowkes FJI,Price JF,Fowkes FGR.Incidence of diagnosed deep vein thrombosis in the general population:systematic review[J].Eur J Vasc Endovasc Surg 2003;25:1–5.
[6] Kahn SR.The clinical diagnosis of deep venous thrombosis:integrating incidence, risk factors,and symptoms and signs[J].Arch Intern Med,1998;158(21):2315–2323.
[7] Kakkar VV,Lawrence D.Hemodynamic and clinical assessment after therapy for acute deep vein thrombosis.A prospective study[J].Am J Surg,1985;15(4A):54-63.
[8] Coon WW.Venous thromboembolism.Prevalence,risk factors,and prevention[J].Clin Chest Med,1984;5(3):391-401.
[9] Viles-Gonzalez JF,Fuster V,Badimon JJ.Thrombin/inflammation paradigms:acloser look at arterial and venous thrombosis[J].Am.Heart.2005;149:(1 Suppl),19-31.
[10] Wakefield TW,Strieter RM.,Prince MR,et al.Pathogenesis of venous thrombosis:a new insight[J].Cardiovasc.Surg.1997;5:6-15.
[11] Springer TA.Traffic signals for lymphocyte recirculation and leukocyte emigration:the multistep paradigm[J].Cell.1994;76:301-314.
[12] Laudanna C,Kim JY,Constantin G,et al.Rapid leukocyte integrin activation by chemokines[J].Immunol Rev.2002;186:37-46.
[13] Furie B,Furie BC,Flaumenhaft RA.A journey with platelet P-selectin:the molecular basis of granule secretion , signalling and cell adhesion [J].Thro -mb.Haemost.2001;86:214-221.
[14] McEver RP.Selectins:lectins that initiate cell adhesion under flow[J].Curr.Opin.Cell Biol.2002;14:581-586.
[15] Geng JG,Chen M,Chou KC.P-selectin cell adhesion molecule in inflammation,thrombosis,cancer growth and metastasis[J].Curr.Med. Chem.2004;11:2153-2160.
[16] Ma YQ,Plow EF,Geng JG.P-selectin binding to P-selectin glycoprotein ligand-1 induces an intermediate state ofαM 2 activation and acts cooperatively with extracellular stimuli to support maximal adhesion of human neutrophils [J].Blood. 2004;104:2549-2556.
[17] Atarashi K,Hirata T,Matsumoto M,et al.Rolling of Th1 cells via P-selectin glycoprotein ligand-1 stimulates LFA-1-mediated cell binding to ICAM-1 [J]. Immunol.2005;174:1424-1432.
[18] Woollard KJ,Kling D,Kulkarni S,et al.Raised plasma soluble P-selectin in peripheral arterial occlusive disease enhances leukocyte adhesion[J].Circ.Res. 2006;98:149-156.
[19] Hamyd AG,Wolf H,Albrecht S.Defective function of peripheral blood monocytes from patients with non-Hodgkin’s lymphoma[J]. Turk.J. Haemato.2001;18:173-178.
[20] Bucek RA,Reiter M.Quehenberger P, et al, The role of solublecell adhesion molecules in patients with suspected deep venousthrombosis. Blood Coagul Fibrinolysis, 2003,14(7):653-657.
[21] Blann AD, Noteboom WM,Rosendaal FR. Increased soluble P-selectin levels following deep venous thrombosis, cause or effect?Br J Haematol,2000, 108(1):191-193.
[22] Polanowska-Grabowska R,Gibbins JM.Gear AR. Plateletadhesion to collagen and collagen-related peptide under flow:rolesof the a2(3t integrin, GP VI,and src tyrosine kinases. ArteriosclerThromb Vasc Biol,2003, 23(10):1934-1940.
[23] Siljander PR, Munnix IC, Smethurst PA, et al. Platelet recepto- rinterplay regulates collagen-induced thrombus formation inflowing human blood. Blood. 2004,103(4):1333-1347.
[24] Yang LC, Wang CJ. Lee TH, et al. Early diagnosis of deep vein thrombosis in female patients who undergo total knee arthroplasty with measurement of P-se[ectin activation, f Vasc Surg, 2002, 35(4):702-712
[25] LoPresti R, Ferrara F, Canino B, et al. Deep venous thrombosis: Leukocyte rheology at baseline and after in vitro activation.Haemostasis, 2000, 30(4):168-173.
[26] Caimi G,Ganino B, Ferrara F, et al. Leukocyte rheology beforeand after chemotactic activation in some venous disease.Eur f Vasc Endovasc Surg,1999,18(5);411-416
[27] Mine S, Tanaka Y, 5uematn M, et al. Hepatocyte growth factoris a potent trigger of neutrophil adhesion through rapid activationof lymphocyte function-associated antigen-1.[J] Lab Invest, 1998,78(11):1395-1404.
[28] Henke PK, DeBrunye 1.A, Sirieter RM,et al. Viral IL.-10genetrans Fer- decreases infiammationand cell adhesion moleculeexpression in a rat model of venous thrombosis.[J] Immunol 2000,164(4):2131-2141.
[29] EvangelistaV,Manarini S,Rotondo S. et al. Platelet/ polymor- phonuclear Leukocyte interaction in dynamic conditions;evidence of adhesion cascade and cross talk between P-selectin and the beta2 integrin CDllb/CD18.[J] Blood1996. 88 (.11):4183-4194.
[30] Goel MS,DiamondSI,.Neutrophil cathepsin G promotesprothrombinase and fibrin formation under flow conditions byactivating fibrinogen- adherent platelets. [J]Biol Chem . 2003. 278(11):9458-9463.
[31] EvangelisV,Manarini S.CollerBS,etal.Roleof P-selectin. beta2- inte- grins,and Src tyrosine kinases in mouse neutrophil-platelet adhesion. [J]Thromb Haemost, 2003. 1(50):1048-1054
[32] Thanaporn P , MyersDD. Wrobleski SK , etal.P-selectininhibition decreases post-thrombotic vein wall fibrosis in a ratmodel. Surgery, 2003,134(2);365-371.
[33] Myers DD,Jr,Henke K ,Wrobleski SK,et al. P-selectin inhibition enhances thrombus resolution and decreases vein wall fibrosis in a rat model. [J]Vasc Surg,2002,36(5):928-938.
[34] Simon DI,Chen I, Xu H, et al. Platelet glycoprotein ibalpha is a counter receptor the leukocyte integrin Mac-1 (CD116/CD18).[J] Exp Med,2000,192(2):193-204.
[35] Wang JS,LiaoCH. Moderate-intensity exercise suppresses platelet activation and poly morphonuclear leukocyte interaction with surface- adherent platelet under shear flow in men. Thromb Haemost,2004. 91(3):587-594.
[1] Nishibori M,Takahashi HK,Mori S.The regulation of ICAM-1 and LFA-1 interaction by autacoids and statins:a novel strategy for controlling inflammation and immune reponses[J].J Pharmacol Sci.2003;92(1):7-12.
[2] WuY,ZhuBD.Effect of DangguiBuxue Decoctiononpro-liferation and expression of interce-llular adhesion molecule-1inhumanumbilicalvein endothelialcells[J].J West China UnivMedSci,2001,32(4):593-595.
[3] ZhangYJ,ZhaoLG,WuXZ.Effect of HuoxuehuayuDe–coctionon expression of adhesivemolecularofintrapulmonicendothelialcellofratssufferedfromSAP[J].ChinTraditHerbDrugs,2001,32(11):1010-1012.
[4] HaoY,QiuQY,WJ. Effect of astragalus poly saccharin(APS) only Mphocyte -endothelium adhesion and th molecu–larmechanism [J]. ImmunnolJ, 2000, 16(3): 206-20.
[5] Ross R.The pathogenesis of atherosclerosis:a perspective for the 1990s[J].Nature 1993; 62(29):801.
[6] Rosenson Rs,Tangeney CC.Antiathero thrombotic properties of stains:implications for cardiovascular event reduction [J].JAMA 1998;279:1643-50.
[7] Peterk,WeirichU,NordtTK,etal.Solublevascular cell adhesion molecule-1(VCAM-1) as potential marker of atherosclerosis[J].Thromb Haemost. 1999;82 Suppl 38-43.
[8] Prksh,Park JH,Kang JS,etal.Involvement of transcription factor sinplasma HDL Protection against TNF-a lpha-induced vascular cell adhesion molecule- 1expression [J].IntJBiochemCellBiol,2003,35(2):168-182.
[9] Codkerill BW, Huehnsty, Weerasinghea, etal. Elevation of plasmahigh-density Lipoprotein concentration reduce sinterleukin-1-induced expression of E-selectin in Aninvivomodel of acutein flammation[J].Circulation,2001,103(1):108-112.
[10] Dmayugap,ZhuJ,Oguchis,etal.ReconstitutedHDLcontaininghuman apolipoprotein A-Ireduces VCAM-1 expression andneointima formation following peria dventitial cuff-induced carotid injury in a poenull mice[J]. Biochem Biophys Res Commun, 1999,264(2):465-468.
[11] CleeM,KasteleinJJ,VandaMM,etal.Ageand residualcholesteroleffluxaffect HDL cholesterollevelsandcoronary artery disease in ABCA1 heterozygotes [J]. J Clin Invest,2000,106(10):1263-1270.
[12] ConnellBJ,GenestJJr.High-density lipoproteins and endothelial function [J]. Circu- lation, 2001,104(16):1978-1983.
[13] ContiCR.Updatedpathophysiologic concept sinunstable coro-nary artery disease [J]. AmHeartJ,2001,141:12-14.
[14] RusHG,VlaicuR,NiculescuF.Interleukin-6 and interleukin-8 protein and gene in human arteriol atherosclerotic wall[J].Atherosclerosis,1996,127:263-271.
[15] SugiyamaS,OkadaY,SukhovaGK,etal.Macropha gemyeloperoxidase regulation by granulocyte macrophagecolony stimulating factor in human atherosclerosis and implication sina-cutecoronary syndromes[J].AmJPathol,2001,158:879-891.
[16] SimoniniA,MoscucciM,MullerDWM,etal.IL-8 is a nangiogenic factor in human coronary atherectomy tissue[J].Circulation,2000,101:1519-1526.
[17] SarenP,WelgusHG,KovanenPT.TNF-a and IL-1 selective lyinduce expression of 92-k Dagelatinase by human macrophages[J].J Immunol,1996,157:4159-4165.
[18]陈利国,屈援,葛红颖,等.补阳还五汤对血瘀证大鼠血管内皮细胞黏附分子表达的影响[J].中草药,2005,36(5):706-708.
[19]王宗仁,李军昌,马爱玲,等.芪丹通脉片对动脉粥样硬化大鼠单个核细胞中细胞间黏附分子1及血管细胞黏附分子1 mRNA表达的影响[J].中国临床康复,2005,9(27):77-9.
[20]龙铟,刘莉,王宗仁,等.中药芪丹通脉片对心肌损伤大鼠血小板功能的影响[J].第四军医大学学报,2003,24(5):406-8.
[21]行利,马静,王宗仁,等.芪丹通脉片对大鼠急性心肌缺血损伤的影响[J].第四军医大学学报,2003,24(5):415-7.
[22]张路,吴宗贵.通心络对实验性家兔主动脉粥样斑块CAM-1表达影响的实验研究[J].中西医结合心脑血管病杂志,2003,1(12):705-706.
[23]陈建宗,田季雨,顾宜,等.复方丹参滴丸对动脉粥样硬化家兔颈动脉血管壁血管细胞黏附分子-1表达的影响[J].中国临床康复,2004,8(24):5048-9.
[24]刘春华,钱冠清,刘会齐,等.银杏叶提取物抑制轻度修饰低密度脂蛋白诱导的血管内皮细胞与单核细胞黏附的实验研究[J].中国中西医结合杂志,2000,20(12):917-9.
[25]赵桂峰,张红霞,范英昌.救心胶囊对损伤内皮细胞黏附因子表达的影响[J].天津中医药,2004,21(2):148-150.
[26]王宗仁,肖铁卉,李晶华,等.芪丹通脉片对肿瘤坏死因子-α诱导的心肌细胞的细胞间黏附分子-1表达的影响[J].中草药,2003,34(11):1035-6.
[27]苗榕生,张晓明,王红彦.醒脑静对急性脑梗塞患者细胞黏附分子及T细胞亚群的影响[J].北京中医药大学学报,2001,24(1):64-71.
[28]陈春富,贾海燕,曹霞,等.黄芪注射液对脑梗死患者外周血细胞黏附分子表达水平的影响[J].解放军医学杂志,2003,28(11):1048-9.
[29]陈根成,胡金城,朱成全,等.益气活血片对脑梗塞大鼠血小板膜黏附分子表达的影响[J].广州中医药大学学报,2003,20(1):48-50.
[30]胡跃强,胡国恒,吴云虎,等.清热化瘀颗粒治疗急性缺血性中风的临床研究[J].山东中医药大学学报,2004,28(1):31-3.
[31]刘萍,章怡祎,张静生.中药复方对损伤人血管内皮细胞表达细胞间黏附分子的影响[J].中国临床康复,2006,10(27):54-6.
[32]刘萍,张静生,郑菲,等.中药对低密度脂蛋白受体基因表达的影响[J].中国中西医结合急救杂志,2000,7(3):141-3.
[33]李树青,刘学英,贺宏.黄芪对冠心病心绞痛的防治作用中国中西医结合急救杂志[J].2002,9(5):270-2.
[34]雷燕,高倩,李悦山,等.黄芪、当归及其组方促血管内皮细胞增殖作用的研究中国中西医结合杂志[J].2002,4(1):21-2.
[35]吴勇,欧阳静萍,涂淑珍,等..黄芪多糖对动脉粥样硬化内皮细胞损伤的影响[J].湖北中医学院学报,2001,13(2):101-3.
[36]姜开余,顾振论,阮长耿.丹参素对CD116、P-selectin、ICAM-1,VCAM-1,E-selectin:表达的影响[J]中国药理学通报,2000,16(6):682.
[37] Chen Y H,Lin S J,Ku H H, et a1.Salvianolic acid Rattenuates VCAM-1 and ICAM-1 expression in TNF-αI-pha-treated huaman aortic endothelial cells.[J]J c cell Biochem, 2001, 82 (3):512
[38]曾素耘,樊素璇,蒋小青.川芎嗪对妊娠高血压综合征患者脐静脉内皮细胞黏附分子表达的抑制作用[J].中华妇产科杂志,2000,35(5):282.
[39]李敏杰,刘勇,马琳,等.葛根素对内皮细胞增殖及黏附分子表达的影响[J].陕西中医,2002,23(2):148.
[40]严群超,莫木顺,甘绍乃,等.葛根素对急性冠脉综合征患者血清可溶性黏附分子的影响[J].辽宁中医杂志,2002,29(6):340.
[41]何玉萍,陈奕芝,方若鸣,等.石菖蒲加冰片对高血脂大鼠血小板活化功能的影响[J].中国中医药科技,2003;10(6):337-8.
[42]沈晓君,魏群.通脉降脂口服液对动脉粥样硬化患者细胞黏附分子表达的影响[J].山东中医杂志,2004,23(10):584-5.
[43]张宇辉,刘国仗.黏附分子和黏附蛋白在冠心病发生发展中的作用[J].心血管病学进展,2000,21(2):113-5.
[44]李兰芳,张建新,兰漫野,等.通脉活血灵胶囊对实验性高脂血症家兔血脂及动脉粥样硬化的影响[J].中草药,2000,31(6):440-2.
[45]李越华,刘宇,顾仁樾.三七有效组分Rx对兔动脉粥样硬化的实验研究[J].中西医结合心脑血管病杂志,2003,1(10):582-4.
[46]孟振行,吴淑敏,孙仁俊,等.丹参防治动脉粥样硬化的机制[J].心脑血管病杂志,1993,12(1):121-3.
[47]周小明,陆再英,汪道文.丹参防治实验性动脉再狭窄及其机制的初步研究[J].中国中西医结合杂志,1996,16(8):480-2.
[48] Bucek RA,ReiterM.Quehenberger P, et al, The role of soluble cell adhesion molecules in patients with suspected deep venous thrombosis[J]. Blood Coagul Fibrinolysis, 2003,14(7):653-7.
[49] Blann AP, Noteboom WM, Rosendaal FR. Increased soluble P-selectin levels following deep venous thrombosis: cause or effect? [J]. Br J Haematol,2000, I08(1):191-3.
[50] LoPresti R, Ferrara F, Canino B, et al. Deep venous thrombosis Leukocyte theology at baseline and after in vitro activation[J].Haemostasis, 2000, 30(4): 168-173.
[51] Caimi G, Gianino B, Ferrara F, et al. Leukocyte theology before and after chemo- tactic activation in some venous disease. [J]. Eur J VasC Endovasc Surg, 1999, 18(5);411-6.
[52] Mine S, Tanaka Y, Suematn M, et al. Hepatocyte growth factor is a potent trigger of neutrophil adhesion through rapid activation of lymphocyte function-associated antigen-1[J]. L.ab Invest, 1998,78(11):1395-1404.
[53] Eppihimer MJ, Schaub RG. P-selectin-dependent inhibition of thrombosis during venous stasis[J]. Arterioscler Thromb Vasc Biol.2000,20( 11):2483-8.
[54] Henke PK, DeBrunye LA, Strietcr RM,et al. Viral IL.-10 genetransfer decreases inflammation and cell adhesion moleculeexpression in a rat model of venous thrombosis[J].JImmunol.2000,164(4):2131-2141.
[55] Konstantopoulos K, Neelamegham S, Burns AR, et al. Venouslevels of shear support neutrophil-platelet adhesion and neutrophilaggregation in blood via P-selectin and bata2-integrin[J].Circulation, 1998, 98(9):873-882.
[56] EvangelistsV,Manarini S, Rotondo S, et al.Platelet/polymorphonuclear leukocyte interaction in dynamic conditions;evidence of adhesion cascade and cross talk between P-selectin andthe beta2 integrin CDllb/CD18[J]. Blood. 1996. 88 (11): 4183-4194
[57] Goel MS,Diamond SI.Neutrophil cathepsin G promotesprothrombinase and fibrin formation under flow conditions by activating fibrinogen-adherent platelets[J]. J Biol C hem.2003.278(11):9458-9463.
[58] Evangelista V,Manarini S. Coller BS, et al.Role of P-selectinbeta2-integrinsand Sre tyrosine kinases in mouse neutrophil platelet adhesion[J]. J Thromh Haemost,2003.1(50):1048 -1054.
[59] Simon DI, Chen I, Xu H, et al. Platelet glycoprotein ibalpha is acounter receptor the leukocyte integrin Mac-1 (CD11b/CD18) [J]. JExp Med。2000, 192(2):193-204.
[60] Babinska A, Kedees MH, Athar H, et al. F11-receptor(F11F/JAM)mediates platelet adhesion to endothelial cells; role ininflammatory thrombosis[J]. Thromb Haemost,2002, 88(5):847-850
[61] Wakefield TW,Strieter RM,Downing LJ,et al. P-selectin andTNF inhibition reduce venous thrombosis inflammation[J]. J SurgRes. 1996, 64(1);26-31.
[62] Myers DD Jr, Hawley AE, Farris DM, et al. Cellular IL-10 ismore effective than viral IL-10 in decreasing venous thrombosis[J].JSurg Res. 2003, 112(2):168-174.
[63]王健,奚九一,张柏根.清营Ⅰ号对深静脉血栓形成形态学演变的实验研究[J].中国中西医结合外科杂志,2003,9(2):116-118.