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Arteriosclerosis sites

Technetium-labelled lipid microspheres were given to patients with ASO (arteriosclerosis obliterans) by intravenous injection, followed by scintigraphy. Technetium accumulated at the sites corresponding to the atherosclerotic lesions (5). [Pg.267]

Urry, D. W. Neutral sites for calcium ion binding to elastin and collagen A charge neutralization theory for calcification and its relationship to arteriosclerosis. Proc. Nat Acad. Sci. (Wash.) 68, 810 (1971)... [Pg.132]

Fig. 2. Proposed process of arteriosclerosis leading to ischemic disease. It is proposed that arteriosclerosis is a process of inflammation within the arterial wall that is initiated by arterial injury (endothelial dysfunction), causing the trapping of lipoproteins (Rll, Zl). These undergo oxidation as proposed in Fig. 1, leading to foam cells saturated with lipid droplets. Continued accumulation of fatty material within the blood vessel wall promotes a fatty streak. Ultimately, there is muscle cell migration and fibrosis leading to a plaque that consists of a fibrous cap with cholesterol crystals and debris within the deep necrotic layer, while inflammatory cells form a dynamic outer edge. It is thought that oxidized lipoproteins can facilitate many of these processes. Mechanical forces predispose the soft outer layer of the plaque to rupture at sites of structural weakness. Rupture of plaques causes thrombosis and incorporation of thrombi into the plaque. Ultimately, a large thrombus appearing in an obstructed vessel can lead to sudden ischemia and unstable coronary syndromes. Fig. 2. Proposed process of arteriosclerosis leading to ischemic disease. It is proposed that arteriosclerosis is a process of inflammation within the arterial wall that is initiated by arterial injury (endothelial dysfunction), causing the trapping of lipoproteins (Rll, Zl). These undergo oxidation as proposed in Fig. 1, leading to foam cells saturated with lipid droplets. Continued accumulation of fatty material within the blood vessel wall promotes a fatty streak. Ultimately, there is muscle cell migration and fibrosis leading to a plaque that consists of a fibrous cap with cholesterol crystals and debris within the deep necrotic layer, while inflammatory cells form a dynamic outer edge. It is thought that oxidized lipoproteins can facilitate many of these processes. Mechanical forces predispose the soft outer layer of the plaque to rupture at sites of structural weakness. Rupture of plaques causes thrombosis and incorporation of thrombi into the plaque. Ultimately, a large thrombus appearing in an obstructed vessel can lead to sudden ischemia and unstable coronary syndromes.
Schwenke, D. C., and Carew, T. E. (1989). Initiation of atherosclerotic lesions in cholesterol-fed rabbits. II. Selective retention of LDL vs. selective inaeases in LDL permeability in susceptible sites of arteries. Arteriosclerosis (Dallas) 9,908-918. [Pg.280]

Dalhnga-Thie GM, Van t Hooft FM, Van Tol A (1986) Tissue sites of degradation of high density hpoprotein apohpoprotein A-IV in rats. Arteriosclerosis 6 277-284... [Pg.61]


See other pages where Arteriosclerosis sites is mentioned: [Pg.858]    [Pg.220]    [Pg.220]    [Pg.511]    [Pg.444]    [Pg.616]    [Pg.1184]    [Pg.192]    [Pg.178]    [Pg.232]    [Pg.1492]    [Pg.165]    [Pg.2]    [Pg.6]    [Pg.24]    [Pg.71]    [Pg.511]    [Pg.264]    [Pg.110]    [Pg.685]   
See also in sourсe #XX -- [ Pg.2 ]




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Arteriosclerosis

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