Abstract
If a mammalian blood vessel is severed, it immediately contracts to limit the flow of blood. Within a few seconds cell-like blood platelets (about 1/8 the diameter of a red cell) touch the cut edges, break down, and aggregate into a plug-like mass. Then, in the stagnant blood near the injury, a complex cascade of proteolytic reactions takes place, resulting in the production of the enzyme thrombin, which changes fibrinogen into fibrin monomer; this polymerizes into fibrin strands which reinforce the platelet plug and form a blood clot. Later the clot contracts and is dissolved, while new cellular growth repairs the wound.
Research supported by Grant 14147 of the National Heart, Lung and Blood Institute.
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References
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© 1978 Springer-Verlag Berlin Heidelberg
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Elliott, D.L. (1978). Mathematical Models of Blood Coagulation Kinetics. In: Mohler, R.R., Ruberti, A. (eds) Recent Developments in Variable Structure Systems, Economics and Biology. Lecture Notes in Economics and Mathematical Systems, vol 162. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-45509-4_7
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DOI: https://doi.org/10.1007/978-3-642-45509-4_7
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