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The main cause of endothelial dysfunction is impaired bioavailability of nitric oxide. [ 1 ] In addition to acting as a semipermeable membrane , the endothelium is responsible for maintaining vascular tone and regulating oxidative stress by releasing mediators, such as nitric oxide, prostacyclin and endothelin , and by controlling local ...
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]
The neutrophils bind to p-ANCAs and subsequently release inflammatory cytokines, reactive oxygen species and lytic enzymes that cause endothelial injury resulting to inflammation and necrosis of the small vessels. [4] The damage that is caused in the kidneys is specifically called necrotizing and crescentic glomerulonephritis. [5]
Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events including stroke, heart disease, and is also present in inflammatory disease such as rheumatoid arthritis, diabetes, and systemic lupus erythematosus. [18] [19] Endothelial dysfunction is a result of changes in endothelial function.
The term inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the body's inflammatory response—the two components are considered together in discussion of infection, and the word is used to imply a microbial invasive cause for the observed inflammatory ...
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.
The chronic endothelial injury hypothesis is one of two major mechanisms postulated to explain the underlying cause of atherosclerosis and coronary heart disease (CHD), the other being the lipid hypothesis. Although an ongoing debate involving connection between dietary lipids and CHD sometimes portrays the two hypotheses as being opposed, they ...
In severe cases, inflammation can lead to sepsis or distributive shock. [11] Vasodilation is also a major component of anaphylaxis. [12] Inflammation causes not only vasodilation but also causes increased vascular permeability, allowing neutrophils, complement proteins, and antibodies to reach the site of infection or damage. [7]