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The endothelium (pl.: endothelia) is a single layer of squamous endothelial cells that line the interior surface of blood vessels and lymphatic vessels. [1] The endothelium forms an interface between circulating blood or lymph in the lumen and the rest of the vessel wall.
Coagulation is a part of an integrated series of haemostatic reactions, involving plasma, platelet, and vascular components. [13] Hemostasis consists of four main stages: Vasoconstriction (vasospasm or vascular spasm): Here, this refers to contraction of smooth muscles in the tunica media layer of endothelium (blood vessel wall).
The smooth muscle cells are controlled by vascular endothelium, which releases intravascular signals to control the contracting properties. When a blood vessel is damaged, there is an immediate reflex, initiated by local sympathetic pain receptors, which helps promote vasoconstriction. The damaged vessels will constrict (vasoconstrict) which ...
Inflammatory and other stimuli (such as hypercholesterolemia) can lead to changes in gene expression in endothelium producing to a pro-thrombotic state. [34] When this occurs, endothelial cells downregulate substances such as thrombomodulin, which is a key modulator of thrombin activity. [35]
Hemodynamic changes (stasis, turbulence): Blood stasis promotes greater contact between platelets/coagulative factors with vascular endothelium. If rapid blood circulation (e.g., because of tachycardia) occurs within vessels that have endothelial injuries, that creates disordered flow (turbulence) that can lead to the formation of thrombosis; [9]
Endothelial activation: As the wound macrophages switches from inflammatory to healing mode, it begins to secrete endothelial chemotactic and growth factors to attract adjacent endothelial cells. Activated endothelial cells respond by retracting and reducing cell junctions, loosening themselves from their embedded endothelium.
Endothelial activation is a proinflammatory and procoagulant state of the endothelial cells lining the lumen of blood vessels. [1] It is most characterized by an increase in interactions with white blood cells (leukocytes), and it is associated with the early states of atherosclerosis and sepsis , among others. [ 2 ]
Any discontinuity detected in the vascular endothelium triggers an automatic response in the clotting system, which in turns stimulates thrombin production. [3] Thrombin also causes platelet aggregation.
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