The ability to prevent blood loss from vessels that have been damaged is an impo

Damage of the subendothelium initiates an intrinsic mechanism within the blood vessel that causes vasoconstriction (vascular spasm). This intrinsic vasoconstriction, coupled with activation of the sympathetic nervous system, reduces blood flow to the region of damage to immediately decrease blood loss. The next step is the formation of the platelet plug. Platelets are fragments of megakaryocytes that circulate within the blood. When tissues are damaged, von Willebrand factor binds to the exposed subendothelium, which stimulates platelet adhesion to the vessel wall. When platelets contact von Willebrand factor, they are activated, which makes them more sticky. Once activated, platelets release several compounds that include serotonin, epinephrine, ADP, and thromboxane A2. Serotonin and epinephrine stimulate further vasoconstriction of the vessels. ADP causes platelets to aggregate. This aggregation stimulates further release of ADP from the platelets and the release of thromboxane A2 which plays multiple roles. Thromboxane A2 stimulates platelet aggregation, ADP secretion, and vasoconstriction. The development of this platelet plug stimulates the formation of a clot. Clot formation requires the interaction between coagulation factors that are present within the blood. The most important coagulation factor is thrombin. Thrombin stimulates the conversion of fibrinogen to fibrin, which forms a meshwork that is stabilized by factor XIII. Prothrombin is converted into thrombin by factor X, which is activated by two independent pathways: intrinsic and extrinsic. The intrinsic pathway involves activating a circulating factor XII by exposure to the subendothelium, which ultimately activates factor X. At the same time, the extrinsic pathway is initiated by damaged tissue release of tissue factor (factor III). This factor complexes with factor VII to activate factor X.