Abstract
Atherosclerosis has been defined as “a variable combination of changes in the intima of the arteries consisting of an accumulation of lipids, complex carbohydrates, blood and blood products, fibrous tissue and calcium deposits, and associated with medical changes” (see Kottke and Subbiah, 1978; Fuster, 1982). Several hypotheses have been introduced in order to explain the pathogenesis of atherosclerosis (see Ross and Glomset, 1976b; Kottke and Subbiah, 1978; Ross, 1981; Fuster, 1982; Gotto, 1985; Ross, 1986). Virchow (1856) and Rokitansky (1852) already focused attention on the possible role of the intima in the pathogenesis of the disease. Virchow believed intimai damage to be a very early step in the development of an atheroma (see Ross, 1981; Fuster, 1982; Gotto, 1985). More recently, these hypotheses have been translated into “the response-to-injury hypothesis”; the basis for this theory lies in the similarity between the development of atherosclerosis and the response of arteries to experimental injury (Ross and Glomset, 1976b; Ross, 1981, 1986).
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Verbeuren, T.J., Herman, A.G. (1988). Endothelium-Dependent Responses and the Release of Endothelium-Derived Relaxing Factor in Atherosclerotic Blood Vessels. In: Vanhoutte, P.M. (eds) Relaxing and Contracting Factors. The Endothelium. Humana Press. https://doi.org/10.1007/978-1-4612-4588-9_22
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DOI: https://doi.org/10.1007/978-1-4612-4588-9_22
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