Platelets are integral to efficient hemostasis because they adhere and aggregate to the sites where tissue factors is exposed by disruption of the vascular endothelial lining. After endothelial cell damage and loss, adhesive glycoproteins such as collagen, thrombin, and von Willebrand factor are exposed in the subendothelial tissue. Receptors on the platelets mediate binding to the glycoproteins, thus causing platelet adhesion to the particular area of vessel injury. An activation process leading to a conformational change in specific glycoproteins enables the platelets to bind multivalent adhesive proteins such as fibrinogen and von Willebrand factor (8). Platelet aggregation occurs through the interaction of adhesive glycoprotein cross-binding two different platelets. The aggregation process continues until the platelets create a hemostatic plug. Activation of platelets leads to (i) increased vasoconstriction through serotonin and thromboxane A2, (ii) vessel wall repair, and (iii) formation of enzyme/cofactor complexes by providing surface membranes upon which blood coagulation complexes can occur (8). Platelets also secrete platelet factor V, a key component of the enzyme/cofactor complex responsible for thrombin production. Thrombin activates more platelets and stimulates further coagulation by initiating fibrin deposition. The fibrin strand deposition reinforces the platelet plug and serves as a site for more von Willebrand factor deposition (9).

0 0

Post a comment