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Endothelial dysfunction may be involved in the development of atherosclerosis [5] [6] [7] and may predate vascular pathology. [ 5 ] [ 8 ] Endothelial dysfunction may also lead to increased adherence of monocytes and macrophages , as well as promoting infiltration of low-density lipoprotein (LDL) in the vessel wall. [ 9 ]
There appears to be a role of cytokines in causing endothelial dysfunction. [3] [4] Finally, according to the "neuropeptide/cerebral vasoconstriction" theory, some specific substances (endothelin 1, thromboxane A2) trigger spasm of the blood vessels with resultant vessel wall damage and edema.
It is characterized by self-reversing episodes during which the endothelial cells which line the capillaries, usually of the extremities, separate for one to three days, causing a leakage of plasma mainly into the muscle compartments of the arms and legs.
Endothelial dysfunction is a result of changes in endothelial function. [20] [21] After fat accumulation and when stimulated by inflammation, endothelial cells become activated, which is characterized by the expression of molecules such as E-selectin, VCAM-1 and ICAM-1, which stimulate the adhesion of immune cells. [22]
The endothelial cells lining the blood vessels become less responsive to vasoconstrictive agents, lose their glycocalyx (normal coating) and negative ionic charge, become leaky and cause extensive over-expression of nitric oxide. [2] The coagulation cascade is also disrupted. [4]
Circulating endothelial cells (CECs) are endothelial cells that have been shed from the lining of the vascular wall into the blood stream. [1] Endothelial cells normally line blood vessels to maintain vascular integrity and permeability, but when these cells enter into the circulation, this could be a reflection of vascular dysfunction and damage. [2]
Acute hepatic dysfunction after TIPS may require emergent closure of the shunt. [citation needed] A rare but serious complication is persistent TIPS infection, also known as endotipsitis. [7] Lastly, the TIPS may become blocked by a blood clot or in-growth of endothelial cells and no longer function.
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 ]