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Fluid Dynamics and Thrombosis

  • Steven M. Slack
  • Winnie Cui
  • Vincent T. Turitto
Part of the NATO ASI Series book series (NSSA, volume 235)

Abstract

Maintenance of blood fluidity and, conversely, arrest of bleeding at sites of vascular injury, depend on complex interactions between clotting factors, platelets, endothelial cells, the subendothelial matrix and proteins of the fibrinolytic pathway. Products generated by one system, e.g., the coagulation cascade, invariably either enhance or inhibit reactions in other pathways. Cleavage of high molecular weight kininogen, for example, amplifies the intrinsic pathway of coagulation and simultaneously releases bradykinin, a peptide with strong vasoconstrictive properties(1). Endothelial cells secrete prostacyclin (PGI2), a potent inhibitor of platelet activity, and both tissue plasminogen activator (t-PA) and t-PA inhibitor, components that play central roles in fibrinolysis(2). In addition, endothelial cells express thrombomodulin, a protein that plays a role in the thrombin-dependent activation of protein C and which ultimately results in the inactivation of Factors Va and VIIIa and release of plasminogen activators(3). Moreover, thrombin generated through the coagulation cascade converts fibrinogen to fibrin, which serves to stabilize developing hemostatic plugs but which also functions as a platelet activating agent.

Keywords

Shear Rate Platelet Adhesion Wall Shear Rate High Molecular Weight Kininogen Platelet Membrane Glycoprotein 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1992

Authors and Affiliations

  • Steven M. Slack
    • 1
  • Winnie Cui
    • 1
  • Vincent T. Turitto
    • 1
  1. 1.Department of Biomedical EngineeringMemphis State UniversityMemphisUSA

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