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Antithrombotic agents

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Abstract

When a blood vessel is breached, liquid blood rushes out until its flow is arrested by a complex three-stage process known as haemostasis [1]. The first two steps are almost instantaneous — a change in vessel tone which produces vasoconstriction; activation of blood platelets so that they can stick to the wound edges and to each other to form the initial haemostatic plug. This plug is then slowly reinforced, as concrete is strengthened by steel wires, by fibrin strands. These are deposited because activation of the clotting system generates thrombin which turns a soluble circulating plasma protein (fibrinogen) into the insoluble threads of fibrin which scaffold the plug. The clotting system is an amplifying cascade whereby substrates are converted into enzymes, which in turn catalyse the conversion of the next substrate. It can be triggered by external thromboplastic materials released from the injured tissues or by activation of clotting factors when they come into contact with injured or foreign surfaces. The first of these coagulation pathways (the extrinsic system, initiated by phospholipid tissue thromboplastins) is more rapid than the contact-activated intrinsic system which may take at least 10 minutes to generate fibrin. A powerful feed-back loop is provided in that the thrombin generated by these processes initiates further platelet and clotting activation to reinforce the plug.

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© 1987 Springer Science+Business Media Dordrecht

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Mitchell, J.R.A. (1987). Antithrombotic agents. In: Hamer, J. (eds) Drugs for Heart Disease. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-3294-5_11

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  • DOI: https://doi.org/10.1007/978-1-4899-3294-5_11

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-0-412-26540-2

  • Online ISBN: 978-1-4899-3294-5

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