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Constituents of the arterial wall

3 CONSTITUENTS OF THE ARTERIAL WALL B6.3.1 Normal arterial wall [Pg.82]

The main constituents of normal human arterial tissues from young adult subjects (20-39 years) are listed in Table B6.4 [20]. The major part of the [Pg.82]

Vessel Diameter Wall thickness (mm) (mm) Length (cm) Blood velocity Reynolds (cm/sec) number  [Pg.82]

Note The data were obtained from a 32-year-old woman who had been free of respiratory disease and died of uremia. For the purpose of description, the pulmonary arterial tree was divided into three zones. [Pg.83]

The composition of normal human arterial tissues is altered with age in many aspects. Table B6.7 lists the observed changes in human aorta, pulmonary and femoral arteries [20]. There is a tendency that both the dry matter and nitrogen content of arterial tissues decreases with age. However, the relative quantity of collagen [22] and elastin [23, 24] in the arterial wall remains almost unchanged with age. Below the age of 39, the wall of human thoracic aorta has 32.1 5.5% elastin, between the age 40-69, the wall contains 34.4 9.3%, and from 70-89, the elastin content is 36.5 10.1 [24]. [Pg.83]


Cholesterol is the central compound m any discussion of steroids Its name is a combination of the Greek words for bile (chole) and solid (stereos) preceding the characteristic alcohol suffix ol It is the most abundant steroid present m humans and the most important one as well because all other steroids arise from it An average adult has over 200 g of cholesterol it is found m almost all body tissues with relatively large amounts present m the brain and spinal cord and m gallstones Cholesterol is the chief constituent of the plaque that builds up on the walls of arteries m atherosclerosis... [Pg.1093]

The major drawback of these classical views is that they fail to take into account the electrical nature of the stable constituents in blood (which are colloidal) and that thrombus formation depends upon factors known to control the aggregation of colloids, namely the electric charge, and its sign and magnitude on the colloids in comparison with that on the arterial walls. [Pg.458]

Although cholesterol is one of the most important physiological constituents in mammals, higher total cholesterol levels, more specifically, increased low-density lipoprotein (LDL) cholesterol levels are known to be a major risk factor of coronary heart disease [4-7]. Elevated levels of circulating cholesterol, specifically LDL cholesterol, result in the migration and penetration of LDL into the arterial walls, and lead to lipid... [Pg.752]

Elastin constitutes the yellow elastic fibers in ligaments, and the outer wall of arteries. It is not affected by dilute acids or alkalies in the cold, but is digested by pepsin and hydrochloric acid. It yields 25 per cent of glycine and 21 per cent of leucine on hydrolysis. Fibroin, which is the chief constituent of the fibers of silk, differs markedly from the other albuminoids and albumins in composition. It contains about 19 per cent of nitrogen, and yields on hydrolysis 36 per cent of glycine, 21 per cent alanine, and 10 per cent tyrosine. [Pg.602]

LDL is one of the major carriers of cholesterol in circulation. LDL is also known as a bad lipoprotein due to the fact that LDL transports cholesterol and other fat molecules to peripheral tissues (i.e. arterial walls) and plays a crucial role in the development of several cardiovascular-related diseases such as atherosclerosis, stroke, and myoeardial infarction. Oleic acid and lysophosphatidylcholine (Figure 5) are the major constituents of LDL. Oxidized LDL (ox-LDL) is rapidly engulfed by macrophages to induce foam cell formation in the arterial wall [37]. Therefore, ox-LDL is thought to be one of the major contributors to the development of atherosclerosis. Moreover, ox-LDL can enhance coronary vasospasm (vasoconstriction) via induce endotheliinn-dependent vasoconstriction consequently preventing vasodilation and increase the activity of protein kinase C isoforms a and 8 in VSMCs of porcine coronary arteries [38-40]. [Pg.6]

Blood and lymphatic vessels are soft tissues with densities which exhibit nonlinear stress-strain relationships [1]. The walls of blood and lymphatic vessels show not only elastic [2, 3] or pseudoelastic [4] behavior, but also possess distinctive inelastic character [5, 6] as well, including viscosity, creep, stress relaxation and pressure-diameter hysteresis. The mechanical properties of these vessels depend largely on the constituents of their walls, especially the collagen, elastin, and vascular smooth muscle content. In general, the walls of blood and lymphatic vessels are anisotropic. Moreover, their properties are affected by age and disease state. This section presents the data concerning the characteristic dimensions of arterial tree and venous system the constituents and mechanical properties of the vessel walls. Water permeability or hydraulic conductivity of blood vessel walls have been also included, because this transport property of blood vessel wall is believed to be important both in nourishing the vessel walls and in affecting development of atherosclerosis [7-9]. [Pg.81]

It is obvious that the main factors involved in atherogenesis are the vessel wall, the constituents of the blood passing through it, and blood flow. To answer the important question of whether or not atherosclerosis is in fact preventable and reversible, it would be necessary to study these factors, and with it, the natural history of the disease in the human. A study of the progress of human arterial disease is much more difficult than in the experimental animal and it must necessarily rest on indirect evidence. [Pg.219]

There are, however, two prevalent concepts on the genesis of atheromatous plaques, the filtration theory and the thrombo-genic theory. They involve different mechanisms and are not easily reconcilable. The filtration theory presumes that plasma constituents enter directly into the arterial wall by a process of diffusion from the lumenal surface of the vessel. Injury to the endothelium and/or intima or a high level of lipoprotein encourages plaque formation. In the other major theory, mural thrombi adhere to the lumenal surface and become incorporated into the wall by an overgrowth of endothelium. The type of plaque formed is dependent upon the ratio of the adhering materials, platelets and fibrin. [Pg.181]

Their results indicated that non-atherosclerotic tissue, non-calcified atherosclerotic plaque and calcified atherosclerotic plaque all give different Raman spectra, and hence this technique can differentiate these three states of a vessel wall. Microscopic Raman spectra were obtained to study the chief constituents of the vessels under examination elastic laminae, collagen fibres, smooth muscle cells, fat cells, foam cells, necrotic cores, cholesterol crystals, p-carotene containing crystals, and calcium mineralisations. The results indicate different levels of each depending on which arterial sample was being observed. For example, calcified atherosclerotic plaques contained a lot more foci of calcium... [Pg.15]

Cholesterol is a principal component of animal cell plasma membranes, and much smaller amounts of cholesterol are found in the membranes of intracellular organelles. The relatively rigid fused ring system of cholesterol and the weakly polar alcohol group at the C-3 position have important consequences for the properties of plasma membranes. Cholesterol is also a component of lipoprotein complexes in the blood, and it is one of the constituents oiplaques that form on arterial walls in atherosclerosis. [Pg.255]

Cholesterol (p. 507), notorious as the substance deposited on the walls of arteries and as the chief constituent of gallstones, is the kind of alcohol called a sterol. Sterols belong, in turn, to the class of compounds called steroids compounds of the general formula... [Pg.514]


See other pages where Constituents of the arterial wall is mentioned: [Pg.83]    [Pg.85]    [Pg.87]    [Pg.83]    [Pg.85]    [Pg.87]    [Pg.83]    [Pg.85]    [Pg.87]    [Pg.83]    [Pg.85]    [Pg.87]    [Pg.458]    [Pg.159]    [Pg.953]    [Pg.309]    [Pg.618]    [Pg.619]    [Pg.406]    [Pg.198]    [Pg.285]    [Pg.45]    [Pg.298]    [Pg.484]    [Pg.375]    [Pg.192]    [Pg.161]    [Pg.502]    [Pg.658]    [Pg.156]   


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