Platelets are necessary for haemostasis, which means prevention of blood loss. There are three mechanisms, and platelets are involved in each.
- Vascular spasm - when a large vessel such as an artery or vein is severed, the smooth muscle in its wall contracts in response to the damage (called the myogenic response). Platelets in the area of the rupture release serotonin, which also brings about vasoconstriction. The diameter of the vessel is thereby made smaller, and the smaller opening may then be blocked by a blood clot. If the vessel did not constrict first, the clot that forms would quickly be washed out by the force of the blood pressure.
- Platelet plugs - when capillaries rupture, the damage is too slight to initiate the formation of a blood clot. The rough surface, however, causes platelets to change shape (become spiky) and become sticky. These activated platelets stick to the edges of the break and to each other. The platelets form a mechanical barrier or wall to close off the break in the capillary. Capillary ruptures are quite frequent, and platelet plugs, although small, are all that is needed to seal them.
- Chemical clotting - The stimulus for clotting is a rough surface within a vessel, or a break in the vessel, which also creates a rough surface. The more damage there is, the faster clotting begins, usually within 15 to 120 seconds. The clotting mechanism is a series of reactions involving chemicals that normally circulate in the blood and others that are released when a vessel is damaged. The chemicals involved in clotting include platelet factors, chemicals released by damaged tissues, calcium ions, and the plasma proteins prothrombin, fibrinogen, Factor 8, and others synthesized by the liver (Thibodeau, 1999).