What are the mechanisms of blood clotting

Blood clotting

Blood clotting, Mechanism for short-term hemostasis, which is controlled in the blood vessels by approx. 30 substances, takes place in different phases and finally leads to the formation of a fibrin clot. After a tissue injury, the Hemostasis initially initiated by the aggregation of thrombocytes (blood platelets) and their adhesion to the wound edges (primary hemostasis). Various factors (von Willebrand factor, platelet activating factor, collagen, thrombin, adrenaline) are involved in this process. In addition, the platelets are deformed and certain receptors on their membrane surface change conformation. The receptors bind to fibrinogen, which means that more and more platelets are linked. At the same time, small amounts of thrombin are produced, which, via reactions with receptors on the platelet membrane, also causes thromboxanes and endoperoxides to be formed via a sequence of reactions, which further intensify the aggregation and deformation of the platelets. Ca. play an important supporting role in all of these processes2+-Ions and ADP (adenosine phosphate). The thrombocytes then release their ingredients (including serotonin, catecholamines, ADP), which have a vasoconstricting effect and stabilize the fibrin bridges, making the aggregation irreversible. So that the platelet aggregation does not go beyond the injury area Prostacyclin released, which binds to the platelets and inhibits aggregation.

During this platelet plug (white deposition thrombus) is formed is secondary hemostasis, the process of Fibrin clotting been initiated to the injured area by the formation of a red deposition thrombus, which also includes erythrocytes, to close completely. The coagulation factors involved are essentially proteolytic enzymes (serine proteases) which are present in the plasma as inactive precursors and which only activate each other in a cascade-like reaction sequence when coagulation is initiated. It is between a extrinsic (Release of the so-called thrombin activator from the injured area) and one intrinsic mechanism (Release of the thrombin activator from the blood through contact of a coagulation factor XII with collagen), but in the case of B. both of them work together (see Fig.). The thrombin formed from prothrombin by the thrombin activator splits the dimeric fibrinogen into two subunits, from which vascular constricting so-called fibrinopeptides are released. The remaining fibrin monomers now polymerize in the presence of a fibrinopeptide, Ca2+Ions and a plasma factor. The bonds between the fibrin molecules are strengthened by the fibrin-stabilizing factor XIII under the action of thrombin and the red deposition plug is created (see Fig.). Excessive clot formation is prevented by the similarly complex process of plasmin-induced fibrinolysis, which dissolves thrombi again. (Thrombosis, hemophilia)



Blood clotting: Scanning electron microscope image of the formation of a fibrin network on the endothelial cells, a process that ultimately leads to the formation of the red separation thrombus. The indented cells are erythrocytes



Blood clotting: Simplified scheme of reactions during blood coagulation (IS = intrinsic system, ES = extrinsic system)