| Popis: |
Platelets circulate in the blood stream in a quiescent state but undergo explosive activation at sites of damage to the blood vessel wall, leading to formation of a haemostatic plug and cessation of bleeding. The quiescent state of the platelet is maintained in part by the inhibitory action of constitutively released nitric oxide from endothelial cells lining the blood vessels. Activation is brought about by contact with extracellular matrix proteins exposed at the site of tissue damage, notably collagen fibres, and is reinforced by release and generation of a large number of substances such as thrombin and thromboxanes. The remarkable number and diversity of these agents facilitates rapid formation of the platelet aggregate leading to arrest of bleeding. Activation of platelets within intact blood vessels, however, can lead to vascular occlusion with subsequent ischaemic tissue damage. In the most severe cases, this leads to myocardial infarction or stroke, two of the major causes of death in the Western world. The platelet, therefore, is a major target for therapeutic intervention in the prevention of thrombotic disease. |
