Role of Macrophages in Regression of Swine Atherosclerosis
Over the years numerous investigators have noted the presence of macrophages or “macrophage-like cells” in arterial lesions in various species in both the progression and regression phases of atherogenesis. Using various combinations of enzyme histochemistry and immune adherence tests on light and/or electron microscopic levels, some information as to the prevalence of cells with at least some of the characteristics of macrophages in regressing lesions has been obtained. Ultrastructurally, Stary (1) documented in rhesus monkeys a rapid decrease in the number of “macrophage-derived foam cells” within four to six months after imposition of a regression diet. These findings are similar to those of Tucker et al (2), who also showed electron microscopically a dramatic decrease in the number of “lipid laden monocytes”.in aortic intimal lesions of rhesus monkeys after a four month regression regimen. Daoud et al (3) showed, in a sequential study of the changes in swine aortic lesions resulting from withdrawal of an atherogenic diet after a six month induction period, that macrophages, numerous in the baseline lesions, first increased in number in the initial six weeks of the regression regimen, then decreased after five and fourteen months of regression until they were rare in the latter period. They were intimately associated with necrosis, and their decrease paralleled the nearly complete disappearance of necrosis by the termination of the experiment. Histochemical demonstration of non-specific esterase on the light microscopic level paralleled these findings (4), showing intensely reactive cells, often near necrotic and/or calcified areas, to be prevalent in the reference and six week regression lesions, more limited at five months and relatively few at fourteen months of regression, when no reaction product-containing macrophages were present in the limited samples available for electron microscopy.
KeywordsEster Hydrolase Cholesteryl Ester Hydrolase Regression Regimen Lesion Macrophage Intimal Smooth Muscle Cell
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