Endothelium

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The entire endothelium approximates 1 kg in weight and provides a surface area approaching that covered by a football field.

It performs a multitude of functions including transport, cell migration, and cytokine secretion.

This cellular surface lining blood vessels produces vasodilators such as nitric oxide, prostacyclin, and. other  vasoactive agents.

It is anti-thrombotic, anti-inflammatory, can sense and respond to signals in the circulation, and allows tissue perfusion.

It’s integrity can be compromised by varying insults: hypertension, smoking, hyperglycemia, hyperlipidemia, hyperuricemia, uremia, and sepsis.

Endothelial function is associated with cardiovascular risk factors including hyperlipidemia, hypertension, diabetes, and advancing age.

Oxidative stress is an important cardiovascular risk factor that increases with age.

Endothelial dysfunction that may result from the above stressors reflects decreased bioavailability of nitric oxide.

Endothelial dysfunction is a hallmark of clinical vascular disease, but it may also be a harbinger of vascular disease.

Endothelial dysfunction is a independent risk factor for future cardiovascular events on any device and is related to arterial function and vascular aging.

And endothelial cells involve their function depending upon their micro environments and can focus on specialized tasks.

Endothelial function can be measured by invasive and noninvasive techniques.

The assessment of coronary endothelial function involves the responses of both the epicardial arteries and the micro circulation to an endothelium-dependent vasodilator such as acetylcholine.

Epicardial coronary artery diameter is measured using coronary angiography or intravascular ultrasound.

 The microvascular endothelium assessment is done with a Doppler or  pressure wire that measures microvasculature endothelial coronary flow reserve.

Non-invasive measurement of endothelial function includes the use of magnetic resonance imaging or positron emission tomography to assess vascular reactivity and measure coronary flow reserve.

Venous plethysmography

 of the forearm, ultrasound of the brachial or radial artery, or digital arterial tonometry measuring vasodilatation by infusion of vasoactive agents such as acetylcholine or nitroglycerin can quantify endothelial dependent and non-dependent vasodilation.

The thin layer of cells that lines the interior surface of blood vessels and lymphatic vessels,

It forms an interface between circulating blood or lymph in the lumen and the rest of the vessel wall.

Endothelial cells form the endothelium are in direct contact with blood are called vascular endothelial celThe endothelial surface is usually smooth and has a selectively permeable vascular barrier.

The endothelial barrier integrity is established by a balance between contractile forces within endothelial cells creating intercellular gaps and the adhesive forces between endothelial cells restricting such gaps.

With injury endothelial cells swell, become activated and more adhesive.

Endothelial cells become rounded, and create gaps allowing fluid and blood cells to exit the vasculature and into the space of Disse.

ls, whereas those in direct contact with lymph are known as lymphatic endothelial cells.

Vascular endothelial cell functions include: fluid filtration, blood vessel tone, hemostasis, neutrophil recruitment, and hormone trafficking.

Endothelium of the interior surfaces of the heart chambers are called endocardium.

The presence of vimentin rather than keratin differentiates endothelial cell from epithelial cells.

Blood and lymphatic capillaries are composed of a single layer of endothelial cells, referred to as a monolayer.

Vascular endothelial cells typically align and elongate in the direction of fluid flow.

Acts as a semi-selective barrier between the vessel lumen and surrounding tissue.

Controls the passage of materials and white blood cells into and out of the bloodstream.

With excessive or prolonged increases in permeability of the endothelial monolayer as in chronic inflammation, tissue edema/swelling may result.

Usually provides a non-thrombogenic surface because it contains heparan sulfate which acts as a cofactor for activating antithrombin

Endothelial dysfunction results in vascular diseases, and is often a key event in the development of atherosclerosis, hypertension, thrombosis, and is often seen in patients with coronary artery disease, diabetes mellitus, hypertension, hypercholesterolemia, as well as in smokers.

Endothelial dysfunction is predictive of future adverse cardiovascular events.

Endothelial dysfunction is present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus.

One of the main mechanisms of endothelial dysfunction is the reduction of nitric oxide.

The major mechanism of endothelial dysfunction is an increase in reactive oxygen species, which can impair nitric oxide production and activity.

Estrogen in early life can be protective and improves endothelial function because of its upregulation of nitrogen oxide, however as estrogen production slows and women become prone to accelerated vascular aging.

Endothelial dysfunction has diagnostic and prognostic significance.

The signalling protein ERK5 has an essential role in maintaining endothelial cell function.

Damaged endothelium releases pathological quantities of von Willebrand factor, which can promote platelet aggregation and adhesion to the subendothelium, and potentially thrombi.

Estimated at least half of women with chest pain and no evidence of coronary artery disease have coronary microvascular dysfunction causing characteristics typical of ischemia.

Shear stress vasculature causes vasodilation owing to endothelium dependent release of nitric oxide.

Endothelial dysfunction occurs at the earliest stage of atherosclerosis characterized by and inbalance in visodilation and vasoconstriction.

Endothelim dysfunction is linked to cardiovascular risk factors such as hypertension, hypoglycemia, smoking,advancing age, polycystic ovary disease, preeclampsia pregnancy an autoimmune diseases.

The noninvasive assessment of endothelial function involves reactive hyperemia with placement of a pressure cuff on the arm and inflation for 5-10 minutes to induce absence of flow and local ischemia: the release of the cuff induces endothelial dependent process of reactive hyperemia that can be quantified and assessed as peripheral endothelial function.

Measurement of peripheral endothelial function correlates with coronary artery endothelial function.

Noninvasive impaired Endothelium function assessment is an independent predictive of future cardiovascular events, as is the function of the endothelium may be a marker  of vascular aging.

In middle-aged women, functional rather than structural coronary abnormalities are a main cause of chest pain syndrome, and it has been shown the coronary flow reserve is lower in women than in men and that contributes to microvascular dysfunction.

In women without coronary artery disease, the presence of endothelial dysfunction is an important predictor of ischemic heart disease.

Conditions that contribute to exhilarate atherosclerosis by inducing and promoting endothelium dysfunction include preeclampsia, polycystic ovarian syndrome, age of menopause, presence of inflammatory sorrows, anemia, hyperuricemia,  and stress induced cardiomyopathy.

The decline in endothelial function starts in early menopause or early menopausal transition and increases after menopause or any period of prolong estrogen deficiency.

Women with spontaneous spontaneous primary ovarian insufficiency are at increased risk for impaired endothelial function and early onset of ischemic heart disease.

Postmenopausal women have a greater than 3 fold risk of atherosclerotic disease when compare with pre-menopausal women.

Vascular health and aging in women is dependent on the hormonal status, and it can be detected by assessing endothelial function, as endothelial function can serve as a marker of vascular aging.

Severe menopausal vasomotor symptoms are associated with hypertension, elevated total cholesterol levels, and increased cardiovascular disease events compared with females with no or a few symptoms suggesting vasomotor symptoms could be related to oxidative stress and adverse cardiovascular disease risk profile.

Endothelial dysfunction has been shown to be prevalent among women with polycystic ovary syndrome, independent of obesity, age, and other risk factors, suggesting a direct vascular effect.

Patients with polycystic ovary disease should undergo noninvasive assessment of endothelial function.

Pregnancy challenges the cardiovascular system with metabolic alterations such as in creased insulin resistance, lipid levels, coagulation and inflammatory factors.

In hypertension in pregnancy, or disorders of gestational diabetes there are vascular endothelial dysfunctions in both the uterine and maternal circulations.

Endothelial dysfunction links preeclampsia and gestational diabetes to the development of cardiovascular disease.

Women with a history of preeclampsia have a twofold increased risk of ischemic heart disease and cerebrovascular disease and fourfold increased risk of developing hypertension.