TF-bearing cells initiate hemostasis
adequate number of functional platelets, an adequate concentration and activity of plasma coagulation and fibrinolytic proteins
Citrated plasma samples are often used in veterinary medicine to determine fibrinogen concentration, activated partial thromboplastin time (APTT), prothrombin time (PT), and d-dimer or fibrinogen degradation product (FDP) concentration
a normally responsive blood vasculature
organ capsules and the adventitia of blood vessel walls.
expressed on fibroblasts and, on cellular activation, on vascular smooth muscle cells, monocytes, and neutrophils.
The TF-bearing cells and platelet surfaces act as the main cellular surfaces for assembly of the procoagulant complexes.
Any vessel injury leads to TF exposure. Factor VII binding to TF results in activation to Factor VIIa.
cell-based, tissue factor (TF)/Factor VII–dependent model of hemostasis
Factor VIIa bound to TF on the cell surface activates Factor IX to Factor IXa
Factor X to Factor Xa
Initially, the formed Factor Xa is limited to the TF-bearing cell, because Factor Xa that diffuses away from the cell is rapidly inhibited by TF pathway inhibitor (TFPI) or antithrombin.
Together with formed Factor Va, Factor Xa is assembled into the prothrombinase complex on the surface of the TF-bearing cell.
An initial small amount of thrombin close to the cell independent of the presence of platelets is generated and is responsible for activation of platelets, release of Factor V from the platelets, activation of Factor V, activation of Factor VIII and release of Factor VIII from von Willebrand factor, and activation of Factor XI.
Platelets also are activated by other mechanisms, including vessel wall collagen and von Willebrand factor, leading to adhesion and aggregation at the injured site.
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