| Circulation of the blood within the cardiovascular system is essential for transportation of gases, nutrients, minerals, metabolic products, and hormones between different organs. It is also essential that blood should not leak excessively from blood vessels when they are injured by the traumas of daily life. Animal evolution has therefore resulted in the development of an efficient, but complex, series of hemodynamic, cellular, and biochemical mechanisms that limit such blood loss by forming platelet-fibrin plugs at sites of vessel injury (hemostasis). Genetic disorders that result in loss of individual protein functions, and therefore in excessive bleeding (e.g. hemophilia), have played an important part in the identification of many of the biochemical mechanisms in hemostasis.
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| It is essential also that these hemostatic mechanisms are appropriately controlled by inhibitory mechanisms, otherwise an exaggerated platelet-fibrin plug may produce local occlusion of a major blood vessel (artery or vein) at its site of origin (thrombosis), or may break off and block a blood vessel downstream (embolism). Arterial thrombosis is the major cause of heart attacks, stroke, and the need for limb amputations in developed countries, but venous thrombosis and embolism are also major causes of death and disability. Clinical use of antithrombotic drugs (antiplatelet, anticoagulant, and thrombolytic agents) is now widespread in developed countries, and requires an understanding of how they interfere with hemostatic mechanisms to exert their antithrombotic effects.
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