Rheological study on coagulation of blood with special reference to the triggering mechanism of venous thrombus formation
Tóm tắt
A markedly reduced blood flow, an elevation of hematocrit and an increased aggregability of erythrocytes [red blood cells (RBCs)] are risk factors for venous thrombus formation (intravascular blood coagulation). However, these risk factors alone seem to be insufficient to stimulate the coagulation cascade in the absence of a primary triggering mechanism. In this paper, our rheological and biochemical studies on blood coagulation, especially focusing on procoagulant activity of RBCs, are summarized. It is shown that the intrinsic coagulation pathway is triggered by the activation of factor IX (F-IX) by RBCs. The F-IX-activating enzyme in normal human erythrocyte (RBC) membranes was purified, identified and characterized. The activation of F-IX by RBCs was enhanced by a decrease in flow shear rate and an elevation in hematocrit. The procoagulant ability of RBCs and coagulation of blood obtained from individuals with a relatively high level of hypercoagulability were enhanced compared with those for normals. The studies demonstrated a new triggering mechanism for coagulation or thrombus formation that may occur under stagnant flow conditions.
Tài liệu tham khảo
Nossel HL, Wilner GD, LeRoy EC. Importance of polar groups for initiating blood coagulation and aggregation of platelets. Nature. 1969;221:75–6.
Davie EW, Fujikawa K, Kisiel W. The coagulation cascade: initiation, maintenance, and regulation. Biochem. 1991;30:10363–70.
Nemerson Y. The reaction between bovine brain tissue factor and factors VII and X. Biochem. 1966;5:601–8.
Rao LVM, Rapaport SI. Activation of factor VII bound tissue factor: a key early step in the tissue factor pathway of blood coagulation. Proc Natl Acad Sci USA. 1988;85:6687–91.
Sevitt S. The structure and growth of valve-pocket thrombi in femoral veins. J Clin Pathol. 1974;27:517–28.
Walsh PN. Platelet-mediated trigger mechanisms in the contact phase of blood coagulation. Semin Thromb Hemost. 1987;13:86–94.
Kawamoto Y, Kaibara M. Reconstituted collagen is not capable of activating factor XII but causes intrinsic coagulation by activating platelets. Blood Coagul Fibrinolysis. 1992;3:371–9.
Mammen EF. Pathogenesis of venous thrombosis. Chest. 1992;102:640–4.
Breddin HK. Thrombosis Virchow’s triad: what is established? Semin Thromb Hemost. 1989;15:237–9.
Thomas DP. Overview of venous thrombogenesis. Semin Thromb Hemost. 1988;14:1–8.
Kawakami S, Kaibara M, Kawamoto Y, Yamanaka K. Rheological approach to the analysis of blood coagulation in endothelial cell-coated tubes: activation of the intrinsic reaction on the erythrocyte surface. Biorheology. 1995;32:521–36.
Iwata H, Kaibara M. Activation of factor IX by erythrocyte membranes causes intrinsic coagulation. Blood Coagul Fibrinolysis. 2002;13:489–96.
Iwata H, Kaibara M, Dohmae N, Takio K, Himeno R, Kawakami S. Purification, identification, and characterization of elastase on erythrocyte membrane as factor IX-activating enzyme. Biochem Biophys Res Commun. 2004;316:65–70.
Kaibara M, Iwata H, Ujiie H, Himeno R, Kaibara M. Rheological analyses of coagulation of blood from different individuals with special reference to procoagulant activity of erythrocytes. Blood Coagul Fibrinolysis. 2005;16:355–63.
McIntire LV. Dynamic materials testing: biological and clinical applications in network-forming systems. Ann Rev Fluid Mech. 1980;12:159–79.
Gerth C, Roberts WW, Ferry JD. Rheology of fibrin clots. II. Linear viscoelastic behavior in shear creep. Biophys Chem. 1974;2:208–17.
Kaibara M. Rheological studies on blood coagulation and network formation of fibrin. Polym Gels Networks. 1994;2:1–28.
Kirkpatric JP, McIntire LV. Dynamic rheological studies of coagulation and fibrinolysis. J Rheol. 1979;23:769–87.
Kaibara M, Kawamoto Y. Rheological measurement of blood coagulation in vascular vessel model tube consisting of endothelial cell monolayer. Biorheol. 1991;28:263–74.
Kaibara M, Date M. A new rheological method to measure fluidity change of blood during coagulation. Application to in vitro evaluation of anticoagulability of artificial materials. Biorheol. 1985;22:197–208.
Murata T, Date M, Kaibara M. Analysis of a newly developed damped-oscillation rheometer: Newtonian liquid. Jap J Appl Phys. 1987;26:1234–40.
Kaibara M, Takahashi A, Kurotobi K, Suzuki Y. Proliferation of endothelial cells on the plasma-treated segmented-polyurethane surface: attempt of construction of a small caliber hybrid vascular graft and antithrombogenicity. Colloids Surfaces B: Biointerfaces. 2000;19:209–17.
Kaibara M, Yotoriyama T, Himeno R. Antithrombogenicity of cultured endothelial cells exposed to blood under stagnant flow conditions. J Jpn Soc Biorheol. 2004;18:52–9.
Colucci M, Balconi G, Lorenzet R, Pietra A, Locati PD, Donati MB, et al. Cultured human endothelial cells generate tissue factor in response to endotoxin. J Clin Invest. 1983;71:1893–6.
Hemker HC, Lindhout MJ, Vermeer C. Blood coagulation factors at phospholipid surfaces. Ann NY Acad Sci. 1977;283:104–13.
Zwaal RFA. Membrane and lipid involvement in blood coagulation. Biochim Biophys Acta. 1978;515:163–205.
Samis JA, Kam E, Nesheim ME, Giles AR. Neutrophil elastase cleavage of human factor IX generates an activated factor IX-like product devoid of coagulation function. Blood. 1998;92:1287–96.
Kawakami S, Kaibara M, Nakayama M, Isogai Y, Ikemoto S, O’Rear EA, et al. Rheological study of the dynamic process of fibrinolysis. Blood Coagul Fibrinolysis. 1997;8:351–9.
Baugh RJ, Travis J. Human leukocyte granule elastase: rapid isolation and characterization. Biochem. 1976;15:836–41.
Takaki A, Enfield DL, Thompson AR. Cleavage and inactivation of factor IX by granulocyte elastase. J Clin Invest. 1983;72:1706–15.
Vikydal R, Korninger C, Kyrle PA, Niessner H, Pabinger I, Thaler E, et al. The prevalence of hereditary antithrombin III deficiency in patients with a history of venous thromboembolism. Thromb Haemost. 1985;54:744–5.
Tsuda M, Miyazaki M, Takada T, Uda Y, Kuzuhara S. A case of protein C deficiency associated with cerebral infarction and obstruction of deep leg and inferior mesenteric veins. Jpn J Psychiatry Neurol. 1993;47:887–92.
Rogers JSII. Hypercoagulable states. West Virginia Med J. 1993;89:61–3.
Gibbs NM. Venous thrombosis of the lower limbs with particular reference to bed-rest. Br J Surg. 1957;45:209–36.
Kaibara M. Thrombus formation and blood flow–Focusing on venous thrombus. Jpn J Soc Biorheol. 2004;18:82–90.
Yasaka M, Beppu S. Hypercoagulability in the left atrium: Part II: Coagulation. J Heart Valve Dis. 1993;2:25–34.
Chien S. Shear dependence of effective cell volume as a determinant of blood viscosity. Science. 1970;22:977–9.
Egeberg O. The blood coagulability in diabetic patients. Scand J Clin Lab Invest. 1963;15:533–8.
Gerbashi FR, Bottoms S, Farag A, Mammen E. Increased intravascular coagulation associated with pregnancy. Obstet Gynecol. 1990;75:385–9.
Hirsh J, Hoak J. Management of deep vein thrombosis and pulmonary embolism. A statement for healthcare professionals. Circulation. 1996;93:2212–45.
Sinzinger H, Karanikas G, Kritz H, O’Grady J. The economy class syndrome -a surgery of 19 cases. VASA. 1999;28:199–203.
Haas S. The risk of venous thrombosis during prolonged travel. Medizinische Welt. 2000;51:28–30.
Rosing J, Tans G, Govers-Riemslag JWP, Zwaal RFA, Hemker HC. The role of phospholipids and factor Va in the prothrombinase complex. J Biol Chem. 1980;255:274–83.
Tracy PB, Nesheim ME, Mann KG. Coordinating binding of factor Va and factor Xa to the unstimulated platelet. J Biol Chem. 1981;256:743–51.
Kaibara M, Shinozaki T, Kita R, Iwata H, Ujiie H, Sasaki K, et al. Analysis of coagulation of blood in different animal species with special reference to procoagulant activity of red blood cell. Jpn J Soc Biorheol. 2006;20:35–43.
Hirsh J. Pulmonary embolism in the elderly. Cardiol Clin. 1991;9:457–74.
Hager K, Setzer J, Vogl T, Voit J, Platt D. Blood coagulation factors in the elderly. Arch Gerontol Geriatr. 1989;9:277–82.
Ibbotson SH, Tate GM, Davies JA. Thrombin activity by intrinsic activation of plasma in vitro accelerates with increasing age of the donor. Thromb Haemost. 1992;67:377–80.
