Question

When a blood vessel is broken, a clot forms. Why does the clot form only at the site of the injury and not systemically?

Answer 1

Hemostasis encompasses a set of tightly regulated processes that govern blood clotting, platelet activation, and vascular repair. The endothelium which resides at the interface between the blood and surrounding tissues, serves an integral role in the hemostatic system.

Upon vascular injury, the hemostatic system initiates a series of vascular events and activates extravascular receptors that act in concert to seal off the damage. Upon blood vessel injury, platelets are exposed to adhesive proteins in the vascular wall and soluble agonists, which initiate platelet activation, leading to formation of hemostatic thrombi.  the endothelium also regulates the recruitment and extravasation of pro-inflammatory leukocytes in response to tissue damage and infection through expression of cell adhesion molecules and cytokines.

Blood clotting is subsequently attenuated by a plethora of inhibitors that prevent excessive clot formation and eventual thrombosis.

Depending on specific tissue needs and local stresses, endothelial cells are capable of evoking either antithrombotic or prothrombotic events.

Healthy endothelial cells express antiplatelet and anticoagulant agents that prevent platelet aggregation and fibrin formation, respectively.

In the face of endothelial dysfunction, endothelial cells trigger fibrin formation, as well as platelet adhesion and aggregation.

While an intact endothelium inhibits the adhesion of platelets, through the release of nitric oxide and prostaglandin I2, activated endothelial cells (which are damaged endothelial cells at the site of vessel leakage) express a variety of molecules and receptors that increase platelet adhesion to the site of injury. In endothelial cells, Weibel-Palade bodies store VWF, P-selectin, angiopoietin-2, t-PA, and endothelin-1, which are active participants of platelet adhesion, leukocyte recruitment, inflammation modulation, fibrinolysis, and vasoconstrictor, respectively.

So, Basically, our body knows when and at which site the clot has to be formed and even the extent of clot that should be formed by the release and signiling of various enzymes and substances which are released or expressed at the site of the injury. Based on the expression and release of substances, the clot is formed at the required site and no clot formation where there is no vessel breakage.

ADDITIONAL INFORMATION-

Endothelial regulation of the blood coagulation system

Under physiological conditions, the endothelium prevents thrombosis by providing a surface that discourages the attachment of cells and clotting proteins.

The endothelium regulates clot formation in part via its activation of the intravascular PARs. PARs exist as four isoforms, PAR-1, PAR-2, PAR-3, and PAR-4, and are expressed in arterial and venous endothelial cells.

Endothelial PARs serve as sensors for proteases and initiate a cascade of cell signals upon activation by thrombin, APC, fXa, the TF/fVIIa/fXa complex, high concentrations of plasmin, and matrix metalloproteases.

An intact and healthy endothelium expresses various anticoagulants, such as TFPI, thrombomodulin, EPCR, and heparin-like proteoglycans.

Endothelial cells also secrete ectonucleotidase CD39/NTPDase1, which metabolizes the platelet agonist ADP, and platelet inhibitors, such as nitric oxide and prostacyclin and prevents clot fromation when there is no damage or leaking of blood.

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