Endothelial damage

Belzer, F.O., Hoffman, R, Huang, J. and Downs, G. (1972). Endothelial damage in perfused dc kidney and cold sensitivity of vascular Na-K-ATPase. Cryobiology 9, 457-460. 

Endothelial damage > Smooth muscle cell damage... 

However, it remains a valid argument (as in the case of atheroma) that increased oxidative stress may be secondary to (rather than a cause of) endothelial damage in hypertension due to other mechanisms. 

Atherogenesis, a persistent inflammatory response that occurs in response to conditions that cause endothelial damage. 

Fig. 11.1. Atherogenesis is a persistent inflammatory response that occurs in response to conditions that cause endothelial damage (e.g., hypercholesterolemia and oxLDL). After endothelial cells are activated, they elaborate cytokines, chemokines, and other mediators that recruit mononuclear cells (monocytes and T lymphocytes) to extravasate into the vessel wall where they are activated and release additional proinflammatory factors. Macrophages are able to take up oxLDL via scavenger receptors causing them to differentiate into foam cells and form a fatty streak that progresses to an atheroma with a necrotic lipid core and a fibrous cap. Chemokines can lead to weakening of the fibrous cap and eventual plaque rupture leading to thrombosis and occlusion of the involved vessel.

Damage to the endothelium of ex vivo corneas after exposure of the epithelial surface to 1.5, 3.0, 6.0, and 12.0% is shown (Fig. 5.15). The ordinate shows the endothelial damage score. The bars over the abscissa refer to the score on days 2 and 7, with the concentrations applied, respectively. Each of the bars over 1.5, 6.0, and 12.0% represents n = 3 experiments. With 3% the endothelia of n = 8 experiments were evaluated. Endothelial damage on day 2 shows a clear dose response. 

Mannucci PM. Von Willebrand factor A marker of endothelial damage Arterioscler Thromb Vase Biol 1998 18 1359-1362. 

Correa RC, Alfieri A. Plasmatic nitric oxide, but not Willebrand factor, is an early marker of endothelial damage, in type 1 diabetes mellitus patients without microvascular complications. Journal of Diabetes and Its Complications 2003, 17, 264-268. 

Physiological effect at the site of an endothelial damage is the conjoint activity of several agonists from exposed subendothelium, released during platelet activation, coming from red or white cells or from activation of clotting mechanisms of the surrounding plasma,... 

Formation of thrombus at the site of endothelial damage. Von Willebrand factor exposed at sites of endothelial damage acts to bind platelets to the vessel wall. Tissue factor, expressed on subendothelial tissue and cytokine-primed macrophages, acts to generate thrombin, which activates platelets and produces fibrin. TFPI, normally present on the endothelial surface, can be released by heparins and can inhibit tissue factor-induced thrombin generation. Abbreviations ADP adenosine disphosphate TFP1, tissue factor pathway inhibitor. 

The presence of foreign materials in the circulation produces activation of the coagulation and the platelet system. Various prothrombotic surfaces have been used to develop experimental animal models. In contrast to many other thrombosis models, the thrombosis induced by foreign surfaces does not presuppose endothelial damage. 

Carotid loops may be associated with aneurysm formation and rarely with embolism, endothelial damage and thrombosis exceptionally there may be focal ischemia on head movement (Sarkari et al. 1970 Desai and Toole 1975). Rarely, these loops may cause hypoglossal nerve lesions or pulsatile tinnitus. 

FLUOROURACIL THALIDOMIDE t risk of thromboembolism Mechanism is uncertain the endothelial damaging effect of fluorouracil may possibly initiate thalidomide-mediated thrombosis Avoid co-administration... 

MITOMYCIN HORMONES AND HORMONE ANTAGONISTS -TAMOXIFEN t incidence of anaemia and thrombocytopenia and risk of haemolytic-uraemic syndrome Mitomycin causes subdinical endothelial damage in addition to the thrombotic effect on platelets caused by tamoxifen, which leads to haemolytic-uraemic syndrome Monitor renal function at least twice weekly during concurrent therapy and watch clinically for bleeding episodes, e.g. nose bleeds, bleeding from the gums, skin bruising... 

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