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The influence of a blood clot in hemodynamics: A meshless method study
Published in J. Belinha, R.M. Natal Jorge, J.C. Reis Campos, Mário A.P. Vaz, João Manuel, R.S. Tavares, Biodental Engineering V, 2019
M.I.A. Barbosa, J. Belinha, R.M. Natal Jorge
An injury of a blood vessel promotes loss of blood. Therefore, an intervention of the hemostatic system is required, in order to repair the wound as fast as possible [6]. Platelets are instantly activated and become capable of strong adhesion to the wall and to each other [6]. The formation of a blood clot normally starts with the exposure of tissue factor and collagen, in the subendothelium, to blood components after a vascular injury [6, 7]. A clot is an aggregation of blood components that becomes pasted up and acts as a barrier to prevent blood loss and reestablishes hemostasis [6, 7]. However, in this process, the small diameter, extended length, degree of curvature, flow characteristics, vessel geometry, flow waveform shape and shape of the inlet velocity profile can influence hemodynamics [8, 9]. Additionally, some pathological phenomena, such as rupture of atherothrombotic plaque or hypercoagulable states, can promote clot formation inside intact vessels, preventing the passage of blood flow (i.e., thrombosis) [7, 10].
Fibrinolytic Enzymes for Thrombolytic Therapy
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Swaroop S. Kumar, Sabu Abdulhameed
Whenever an injury or trauma occurs, the blood flow through the vessels should be immediately arrested to prevent the loss. This is achieved by hemostasis, characterized by equilibrium between blood coagulation and fibrinolysis. The hemostatic system includes primary hemostasis (platelet plug formation), secondary hemostasis (coagulation), and tertiary hemostasis (fibrinolysis). Primary hemostasis initiates through vascular spasm or local vaso-constriction occurring immediately after injury and thereby reducing the blood flow through the vessel followed by platelet aggregation to form platelet plug. Coagulation factors normally exist as pro-enzymes and circulate through blood stream along with pro-coagulant and anticoagulant factors such as von Willebrand factor (vWF), tissue factor, platelet activating factors, tissue factor pathway inhibitor, endothelium-derived relaxing factor or nitric oxide (NO), tissue plasminogen activator (t-PA) and prostacyclin (Lane et al., 2005; Pearson, 1994). Once trauma occurs, the above factors get activated. Coagulation or secondary hemostasis usually referred as coagulation cascade initiates a series of enzyme reactions which consists of intrinsic and extrinsic pathways (Macfarlane, 1964). Chief coagulating enzyme thrombin, formed from Factor Xa initiates fibrin polymerization and thereby blood clotting (Kovalenko et al., 2017). However, removal of clot after wound healing is also important in order to ensure the proper blood circulation. Tertiary hemostasis is characterized by the dissolution of clot or fibrinolysis controlled by fibrinolytic system. Plasmin is the enzyme that degrades clot, and it is formed form plasminogen with the aid of plasminogen activators. However, this is regulated by plasminogen activator inhibitor 1 (PAI-1), thrombin-activatable fibrinolysis inhibitor (TAFI), α2-antiplasmin and α2-macroglobulin, etc. (Stassen et al., 2004).
In vitro Evaluation
Published in Raj Bawa, János Szebeni, Thomas J. Webster, Gerald F. Audette, Immune Aspects of Biopharmaceuticals and Nanomedicines, 2019
The prothrombin time (PT) test measures the activation of coagulation by the extrinsic or tissue factor. For the assessment of the coagulation time, once a sample is placed into the coagulometer, phospholipid calcium thromboplastin is added and the coagulation time is automatically assessed. Normal values for healthy humans are in the range 12–15 s.
Platelet adhesion potential estimation in a normal and diseased coronary artery model: effects of shear stress magnitude versus shear stress history
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
The adhesion and thrombotic molecules of interest in this study are tissue factor, CD41a, CD42b and CD62P. Tissue factor is expressed on activated vascular cells and is a major regulator of the extrinsic coagulation pathway (Houston et al. 1999). CD41a (GPIIb) is necessary for platelet aggregation to fibrin and clot formation (Liu et al. 2009). CD42b (GPIba) interacts with von Willebrand factor and therefore plays a role in platelet adhesion (Fuchs et al. 2010). CD62P (P-selectin) is associated with platelet activation and plays a role in leukocyte recruitment and adhesion (Wein et al. 1995). Each of these molecules plays an important role in CHD development and progression.