Smoking, Catecholamines and their Effects on Endothelial Cell Integrity
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Atherosclerosis is not uniformly distributed over the arterial surface. The preferential localization of atherosclerotic lesions to areas close to branching points and curvatures suggests that hemodynamic strain may be involved in the initiation of atherogenesis. The actual link between hemodynamic strain and atherogenesis has not been defined, but already Virchow (1856) suggested that injury imposed by the wear and tear of flow might be of significance. When Virchow’s ideas were revitalized in the later sixties and early seventies (Baumgartner and Studer 1966, Björkerud 1969, Bondjers and Björnheden 1970, Stemerman and Ross 1972) the primary emphasis was placed on injury in the form of endothelial denudation. When the subendothelial tissue was exposed by removal of the endothelium, platelets adhere and release growth factors. These growth factors, and in particular PDGF, stimulate underlying smooth muscle cells to proliferate (review with references: Ross 1981) to form an intimai thickening. This concept, the original response-to-injury hypothesis has recently been challenged (reviews with references: Reidy and Schwartz 1984, Reidy 1985). Thus, it has been difficult to demonstrate significant endothelial denudation with exposure of subendothelial tissue in the absence of mechanical injury, and even when such injury is induced smooth muscle proliferation does not necessarily follow.
KeywordsTobacco Smoke Cynomolgus Monkey Endothelial Injury Integrity Behavioral Smooth Muscle Proliferation
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