Biomedical Engineering Reference
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Fig. 3.3. Typical curve illustrating the time behaviour of Thrombin concentration during the clot-
ting process
Thrombin from its precursor FXIII (also known as Laki-Lorand factor), which acts
on polymerized Fibrin, stimulating the formation of cross links in the network (see
Fig. 3.4). The importance of the latter stage is confirmed by the bleeding disorder
associated to FXIII deficiency.
Termination
Stopping the self exciting mechanism of clotting is as important as initiating it
(Fig. 3.5). Here too, Thrombin has a key role. We have already seen (see initiation
phase) that the complex Thrombin-TM helps confining the clot growth at the injury
site. This complex has two opposite effects on the clot. One is to contrast fibrino-
lysis (see the next subsection), the other is to give rise to the APC-ProS complex,
possessing an inhibiting action on FVa and FVIIIa, so that no more Prothrombinase
can be produced, interrupting the coagulation process. In the paper [86] the author
questions the real ability of APC-ProS to neutralize FVa far from endothelial cells,
leaving some doubt on the actual termination mechanism.
Fig. 3.4. Cell-based model: Propagation phase of blood coagulation
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