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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.
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 ...
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).
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]
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 ]
Vascular sprouting: With the breakdown of endothelial basement membrane, detached endothelial cells from pre-existing capillaries and post-capillary venules can divide and migrate chemotactically towards the wound, laying down new vessels in the process. Vascular sprouting can be aided by ambient hypoxia and acidosis in the wound environment ...
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.
Neither did he ever suggest a triad to describe the pathogenesis of venous thrombosis. In fact, it was not until decades after Virchow's death that a consensus was reached proposing that thrombosis is the result of alterations in blood flow, vascular endothelial injury, or alterations in the constitution of the blood.