<![CDATA[<a rel="nofollow" href="https://http://www.mhhe.com/biosci/esp/2002_general/Esp/folder_structure/tr/m1/s7/assets/flash/trm1s7_3.swf" target="_blank">https://http://www.mhhe.com/biosci/esp/2002_general/Esp/folder_structure/tr/m1/s7/assets/flash/trm1s7_3.swf</a>]]>Damage to small blood vessels and capillaries frequently occurs. When these vessels are damaged, there are three basic mechanisms that promote hemostasis or the stoppage of bleeding.
Following damage, there is an immediate reflex that promotes vasoconstriction, thus diminishing blood loss. Exposed collagen from the damaged site will promote the platelets to adhere.
When platelets adhere to the damaged vessel, they undergo degranulation and release cytoplasmic granules, which contain serotonin, a vasoconstrictor, and ADP and Thromboxane A2.
The ADP attracts more platelets to the area, and the thromboxane A2 promotes platelet aggregation, degranulation, and vasoconstriction. Thus ADP and thromboxane A2 promote more platelet adhesion and therefore more ADP and thromboxane. The positive feedback promotes the formation of a platelet plug.
The final hemostatic mechanism is coagulation.
Damaged tissue releases factor III, which with the aid of Ca++ will activate factor VII, thus initiating the extrinsic mechanism. Factor XII from active platelets will activate factor XI, thus initiating the intrinsic mechanism.
Both active factor VII and active factor XI will promote cascade reactions, eventually activating factor X.
Active factor X, along with factor III, factor V, Ca++, and platelet thromboplastic factor (PF3), will activate prothrombin activator.
Prothrombin activator converts prothrombin to thrombin.
Thrombin converts fibrinogen to fibrin.
Fibrin initially forms a loose mesh, but then factor XIII causes the formation of covalent cross links, which convert fibrin to a dense aggregation of fibers. Platelets and red blood cells become caught in this mesh of fiber, thus the formation of a blood clot.
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