Thrombozytenaggregationshemmer

Thrombozytenaggregation, commonly referred to as platelet aggregation, is a critical hemostatic process involving the adhesion and activation of platelets, leading to the formation of a platelet plug. This plug is essential for sealing damaged blood vessels and preventing excessive bleeding. The process is initiated when a blood vessel wall is injured, exposing collagen and tissue factor. Platelets circulating in the blood then adhere to the exposed subendothelial matrix, primarily through the binding of von Willebrand factor (vWF) to platelet glycoprotein Ib (GPIb) receptors.

Upon adhesion, platelets undergo activation. This activation triggers a conformational change in the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor, increasing its affinity for fibrinogen. Activated platelets release various mediators, including adenosine diphosphate (ADP) and thromboxane A2 (TXA2), which further recruit and activate nearby platelets. These recruited platelets also adhere and activate, amplifying the aggregation process. Fibrinogen then acts as a bridge, binding to the activated GPIIb/IIIa receptors on adjacent platelets, thereby cross-linking them and forming a stable platelet aggregate. This aggregate, along with fibrin, forms a thrombus that occludes the injured site. Dysregulation of platelet aggregation can lead to either bleeding disorders or thrombotic events, such as heart attack and stroke.