Platelet adhesion is a part of hemostasis in which platelets attach to collagen. This step activates platelets.
What is platelet adhesion?
Platelet adhesion is a part of hemostasis in which platelets attach to collagen. Shown in white in Figure Platelet or blood platelets. Primary hemostasis – hemostasis – occurs in 3 phases. The first step is platelet adhesion, followed by reversible platelet aggregation and formation of an irreversible platelet plug. The role of hemostasis is to repair injured vessels as quickly as possible to minimize blood loss. That is why vasoconstriction occurs immediately when the endothelium is injured. The constriction of the vessels also results in slower blood flow. This supports the next step: Platelet adhesion. In this process, the platelets (thrombocytes) attach themselves to subendothelial structures, such as collagen. This adhesion is initiated directly by the collagen receptor and indirectly by the so-called von Willebrand factor. The adhesion activates platelets and reversible platelet aggregation is initiated. Thus, platelets adhere tightly to each other, and eventually an irreversible platelet plug is formed.
Function and role
The function of platelet adhesion is an interaction of von Willebrand factor with various glycoproteins. At the molecular level, it is a ligand-receptor interaction. Ligand is the so-called von Willebrand factor and the most important platelet receptor is the GP Ib/IX complex. Platelet attachment to subendothelial surfaces is mediated by the GP Ia/IIa receptor complex – the collagen receptor. Indirectly, von Willebrand factor (vWF) also has an influence. This is a large glycoprotein released from the injured endothelium. It can form bridges between special membrane receptors of platelets (GP Ib/IX complex) and collagen fibers. Fibronectin and thrombospondin are also involved in this bridge formation. The exposed collagen structures additionally interact with GP Ia/IIa and GP VI on the platelet surface without the vWF. Both reactions contribute to platelet rolling along the vessel wall and eventual adhesion. In conclusion: The collagen receptor leads to a single-layer platelet lawn. The von Willebrand factor causes firm attachment of platelets via GP Ib/IX forms. This platelet adhesion, in combination with vasoconstriction, leads to an initial reduction in bleeding. In addition, it is important for platelet activation. Platelet activation additionally involves the release of adenosine diphosphate (ADP), fibrinogen, fibronectin, vWF, and thromboxane A2. Platelet activation initiates reversible platelet aggregation. Platelets closely adhere to each other via fibrinogen bridges. Vasoconstriction is further enhanced by the leakage of blood plasma into the interstitium. Thrombin causes the platelets to fuse into a homogeneous mass, the irreversible platelet plug. The formation of the irreversible platelet plug and vasoconstriction ensure that temporary hemostasis occurs within a short time in small injuries. Primary hemostasis can be inhibited pharmacologically. Such as by acetylsalicylic acid (e.g. aspirin), which suppresses the synthesis of thromboxane A2. Other platelet function inhibitors include ADP and GP IIb/III a antagonists. These drugs are often used temporarily in bedridden patients, such as before and after surgery. Their purpose is to inhibit blood clotting and thereby prevent thrombosis and embolism. This procedure is called thromboprophylaxis.
Diseases and medical conditions
The tendency of platelets to adhere (adhesiveness) can be measured using defined glass surfaces or on glass bead filters (retention). Inadequate platelet adhesion function is manifested primarily by increased bleeding tendency. Platelet adhesion disorders are hereditary. They are based on a disturbed interaction between platelets and the vascular endothelium. The cause of this disorder can be, for example, a deficiency of the von Willebrand factor, as is the case in Willebrand-Jürgens syndrome. This disease is inherited in almost all cases.Acquired forms have been described only very rarely. The manifestation and severity of the syndrome can vary. There are often very mild courses of the disease, so that the disease often even remains unnoticed for a long time. Roughly, 3 types of the disease can be distinguished. In type I, there is a quantitative deficiency of von Willebrand factor. This form is the most common, it shows very mild symptoms and often allows patients to lead a normal life. Only the bleeding time is somewhat longer, and patients suffer more often from postoperative bleeding. In type II, on the other hand, there is a qualitative defect in the Willebrand factor. This form is the second most common, but affects only 10-15% of all patients with Willebrand-Jürgens syndrome. Type III has a very severe course, but is the rarest. The disease is diagnosed in the laboratory in the presence of corresponding symptoms. Here, the amount and activity of von Willebrand factor is measured. Permanent therapy is usually not necessary at the time of diagnosis. Only before operations are affected patients given desmopressin, which increases the amount of von Willebrand factor fivefold. Bernard-Soulier syndrome, on the other hand, occurs much less frequently. Here, the disorder of platelet adhesion is due to a hereditary defect of the membrane receptor for von Willebrand factor (GP Ib/IX). This disease is also associated with an increased bleeding tendency. However, spontaneous bleeding is rare. The diagnosis is again made in the laboratory, and therapy is also rarely required due to the mild symptoms. Patients need only be careful not to take antiplatelet drugs, such as aspirin. These can lead to severe bleeding complications. Platelet concentrates are substituted only in acute cases, such as after major blood loss.
