Platelet aggregation

When a vessel is injured, the platelets come into contact with the connective tissue, which normally has no contact with the blood. A coagulation factor, the so-called von Willebrand factor (vWF), can now attach itself to this tissue from the blood. The thrombocyte has special receptors for this factor (vWR) and binds to it.

This leads to attachment of the thrombocytes, also known as adhesion. This is also the stimulus for the thrombocytes to activate them. They change their disc shape and form many extensions (pseudopodia).

They also release the contents of their granules, which contain coagulation factors and other platelet-activating substances. The latter include for example adenosine diphosphate (ADP) or thrombboxane. This triggers a kind of chain reaction so that many more platelets can be activated.

The activation of the thrombocytes also leads to a change in the shape of the GPIIb/IIIa protein on their surface. This protein functions as a receptor for a plasma protein called fibrinogen. It acts as a bridge between platelets and connects them with each other via GPIIb/IIIa.

This means that a network of platelets linked by fibrinogen can form at the site of injury. This network is called the “white platelet thrombus” and the process is called platelet aggregation. As the process continues, the coagulation factors of secondary hemostasis are activated and a very stable cross-linked thrombus is formed.

Platelet aggregation inhibitor

For some diseases or conditions platelet aggregation must be inhibited. One option is the well-tried ASS (acetylsalicylic acid), which inhibits an enzyme (COX-1) that produces the thrombboxane necessary for aggregation. In addition, the receptor molecules of the thrombocytes can also be inhibited.

So-called ADP-receptor blockers (synonym: P2Y12-receptor blockers) can also prevent an activation of the thrombocytes by the adenosine diphosphate. These include clopidogrel or ticagrelor, for example. Last but not least, the cross-linking of the thrombocytes via the receptor called GPIIb/IIIa can be prevented. Abciximab, for example, is one of these drugs that unfortunately cannot be taken orally.