Intima of arteries

Fibrosis resulting in the loss of normal organ structures is the hallmark of chronic rejection. The fibrosis may be due to wound healing, which is then followed by the cellular necrosis of acute rejection. However, it must be pointed out that chronic rejection develops many times in the absence of acute rejection. Fibrosis may be a result of several diverse factors such as equation of chronic rejection with chronic delayed-type hypersensitivity reaction, injury to blood vessels and resulting response to chronic ischemia, the proliferation of smooth muscle cells in the intima of arterial walls producing vascular occlusion, or persistent viral infections that will induce cellular immune response. 

Atherosclerosis involves the formation of lipid-rich plaques in the intima of arteries. The plaques begin as fatty streaks containing foam cells, which initially are macrophages filled with lipids, particularly cholesterol esters. These early lesions develop into fibrous plaques that may occlude an artery and cause a myocardial infarct or a cerebral infarct. Formation of these plaques is often associated with abnormalities in... 

Atherosclerosis (athero = fatty and sclerosis = scarring or hardening) of the coronary and peripheral vasculature is the leading cause of morbidity and mortality worldwide. Lesions (called plaque) are initiated by an injury to endothelium and thicken the intima of arteries, occlude the lumen, and compromise delivery of nutrients and oxygen to tissue (ischemia). Atherosclerotic lesions primarily occur in large and medium-sized elastic and muscular arteries and progress over decades of life. These lesions cause ischemia, which can result in infarction of the heart (myocardial infarction) or brain (stroke), as well as abnormalities of extremities. The proximate cause of occlusion in these pathological conditions is thrombus formation. 

The term atherosclerosis refers to the focal thickening of the intima of arteries. " The thickened intima consists of muscle cells, connective tissue such as collagen and elastin, mucopolysaccharides, and both intracellular and extracellular lipids. As it progresses to the more advanced condition, degenerating cells and cholesterol crystals are found in the lesions. Plasma proteins, lipoproteins, and the formed elements of blood (platelets, leukocytes, and erythrocytes) are also involved in the development of lesions. Progressive atherosclerosis leads to poor blood flow through blood vessels due to occlusive complications, which also promote the accumulation of formed elements. 

Introduction - Atherosclerosis is defined by the WHO "as a variable combination of changes of the intima of arteries consisting of the focal accvimulation of lipids, complex carbohydrates, blood and blood products, fibrous tissue and calcium deposits and associated with medial changes." Once formed the advanced plaque seldom regresses, and consequently major research attention has concentrated on prevention of additional deposits or, in the longer view, on the primary prevention of all lesions. 

The oxidation hypothesis that oxidatively modified LDL particles are retained in the intima of arteries leading to atherosclerosis is supported by considerable evidence, but remains unproven. The inflammation hypothesis has recently been emphasized in the mediation of all stages of atherosclerosis including initiation, and acute thrombotic complications of atheroma. Since many lipid oxidation products are pro-inflammatory, the inflammation and oxidation hypotheses are closely linked. Oxidized LDL and the oxidized phosphatidylcholine components of LDL are in fact pro-inflammatory and have proatherogenic properties. In addition to LDL, other lipoprotein particles including VLDL and a subfraction called beta VLDL and IDL may undergo oxidation, activate inflammation and become atherogenic. 

Atherogenesis. Formation of atheromas, plaques in the intima of arteries that narrow the arterial passage, restricting blood flow and increasing the risk of... 

A large fraction of the cholesterol present in lymph and blood plasma is found in the chylomicrons and about two-thirds of the plasma cholesterol is esterified with fatty acids giving cholesteryl esters. Cholesterol and its esters constitute a large fraction of the lipid present in the atheromatous plaques which are deposited in the intima of arteries in the condition of atherosclerosis (page 267). Cholesterol, which is insoluble in aqueous media, is also a major constituent of most gallstones. 

Aneurysms Abnormal bulging or dilatation of a segment of a blood vessel or myocardium. Artery Blood vessel transporting blood in a direction away from the heart. Atherosclerosis Lipid deposits in the intima of arteries. 

Diseases. Liquid crystals have been impHcated in a number of disease conditions in the human body. A complex cholesterol—phosphoHpid—Hpoprotein Hquid crystal phase has been identified in the initiation and maintenance of atheromatous deposits on the aortic intima in dissected human and rabbit arteries (40). The paracrystalHne nature of this precursor to plaque buildup with the resultant loss of arterial elasticity... 

The intima of the arterial wall contains hyaluronic acid and chondroitin sulfate, dermatan sulfate, and heparan sulfate proteoglycans. Of these proteoglycans, dermatan sulfate binds plasma low-density lipoproteins. In addition, dermatan sulfate appears to be the major GAG synthesized by arterial smooth muscle cells. Because it is these cells that profiferate in atherosclerotic lesions in arteries, dermatan sulfate may play an important role in development of the atherosclerotic plaque. 

Although atherosclerosis and rheumatoid arthritis (RA) are distinct disease states, both disorders are chronic inflammatory conditions and may have common mechanisms of disease perpetuation. At sites of inflammation, such as the arterial intima undergoing atherogen-esis or the rheumatoid joint, oxygen radicals, in the presence of transition-metal ions, may initiate the peroxidation of low-density lipoprotein (LDL) to produce oxidatively modified LDL (ox-LDL). Ox-LDL has several pro-inflammatory properties and may contribute to the formation of arterial lesions (Steinberg et /., 1989). Increased levels of lipid peroxidation products have been detected in inflammatory synovial fluid (Rowley et /., 1984 Winyard et al., 1987a Merry et al., 1991 Selley et al., 1992 detailed below), but the potential pro-inflammatory role of ox-LDL in the rheumatoid joint has not been considered. We hypothesize that the oxidation of LDL within the inflamed rheumatoid joint plays a pro-inflammatory role just as ox-LDL has the identical capacity within the arterial intima in atherosclerosis. 

Atherosclerosis is a pathogenic response of the intima of the arterial vessel walls to noxious stimuli. It is characterized by lipids depositing in the vessel walls, which leads to wall narrowing. This can progress to IHD. Exposure to arsenic in drinking water is associated with an increased prevalence of carotid atherosclerosis in a dose-response relationship. In a cross-sectional study, Wang et al. (2002) assessed... 

Hanke H, Strohschneider T Oberhoff M, Betz E, Karsch KR, Time course of smooth muscle cell proliferation in the intima and media of arteries following experimental angioplasty, Circ Res 1990 67(3) 651-659. 

Atherosclerosis Common form of arteriosclerosis with deposits of yellow plaques containing cholesterol, lipid material within the intima and inner media of arteries. 

The level of oxidative protein modifications may indicate oxidative stress in normal and pathological conditions. Increased content of carbonyl groups was found in diffusely thickened intima (neointima) of arterial walls in arteriosclerotic tissues (M19). Comparison of oxidatively modified amino acids content in normal intima and in human carotid plaque samples revealed an increased content of 3-chlorotyrosine, DOPA, o-tyrosine, m-tyrosine, hydroxyleucine, hydroxyva-line, and especially, dityrosine (F17, H13). These plaques are indicative of the role of protein oxidative damage in the formation of atherosclerotic plaques. Postmortem studies revealed that the content of dityrosine is increased in the stage of advanced lesions. However, the o-tyrosine and m-tyrosine are not elevated in plaque proteins (H13, LI 1). The question of 3-nitrotyrosine level in atherosclerotic plaques remains unresolved, the reported data being contradictory (E6, L10, M24). 

Rubba P, Mercuri M, Faccenda F et al. (1994). Premature carotid atherosclerosis does it occur in both familial hypercholesterolemia and homocystinuria Ultrasound assessment of arterial intima-media thickness and blood flow velocity. Stroke 25 943-950 Rubinstein SM, Peerdeman SM, van Tulder MW et al. (2005). A systematic review of the risk factors for cervical artery dissection. Stroke 36 1575-1580... 

Diseases of elastic tissue are few compared with those that affect collagen, and in these destruction of preformed elastic fibers appears to occur only in localized areas, particularly in the walls of blood vessels and in the skin. In arteriosclerosis loss of elasticity and breakdown in the structure of the elastic elements in the media of arteries is accompanied by calcification of the media and the development of calcified plaques in the intima. Since calcification of the media may be seen to occur without the development of atheromata, it is thought that this change may be associated in the first place with age. Other age-related changes looked for have been changes in the gross content of elastin in the media and changes in the amino acid... 

Atherosclerosis is a major cause of death in most industrial societies. The characteristic lesion of this disease, the atherosclerotic plaque, is found in the intima of large- and medium-sized arteries. An additional problem with advanced plaques is that thrombus formation is likely to occur in regions of plaque rupture. The combination of the two events can lead to partial or even total occlusion of major arteries. If this occurs in one or more of the coronary arteries, a serious or even fatal MI may result. A discussion of arteriosclerosis and exogenous agents that can modulate this condition is presented below. 

Free radical damage is considered to be a causative factor in the development of cancer and inflammatory and chronic diseases. Therefore, free radical scavenging molecules (antioxidants) may play a beneficial role in these conditions. With repect to CVD, the oxidation of low-density lipoprotein (LDL) is believed to be a critical process in the development of atherosclerosis (Berliner et al., 1995 Navab et al., 1995). The presence of oxidized LDL in the intima of an artery leads to the production of macrophage-derived foam cells, the main cell type present in fatty streaks that are believed to be the earliest lesion of atherosclerosis (Fuster, 1994). Therefore, the use of antioxidants as dietary supplements to protect against LDL oxidation may reduce both the development and progression of atherosclerosis (Gey, 1995). 

The normal artery wall is composed of three layers intima, media, and adventita (Figure 20-10). On the luminal side, the intima contains a single layer of endothelial cells. These cells permit passage of water and other substances from blood into tissue cells. On the peripheral side, the intimal layer is surrounded by a fenestrated sheet of elastic fibers (the internal elastic lamina). The middle portion of the intimal layer contains various extracellular components of connective tissue matrix and fibers and occasional smooth cells, depending on the type of artery, and the age and sex of the subject. 

Atherosclerosis is the progressive accumulation of cholesterol, inflammatoiy and other cells, and extracellular matrix in the subendothelial space (intima) of an artery wall, ultimately leading to the formation of a plaque that can occlude the lumen (see Figure 18-19). 

Atherosclerosis is believed to be predominantly an inflammatory condition produced as a response to injury (Elkind, 2006). Atherosclerosis is defined by the accumulation in the arterial intima of mainly low-density lipoprotein (LDL)-derived lipids along with apolipoprotein B-lOO (apoBlOO). LDL is the major carrier of cholesterol in the circulation and is composed of one apoB-100 together with phosphatidylcholine (PC), sphingomyelin (SM) and unesterified cholesterol (500 200 400 molecules respectively) constituting a surface film surrounding a core of cholesteryl esters and triacylglycerols. 

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