Abstract
Macroscopically lesion-free parts of human aortas with no or light lesions (group I) and advanced atherosclerotic lesions (group II) were submitted to a series of successive extractions in order to "solubilize" all the macromolecular components of the arterial wall ("chemical dissection"). Lipids were extracted with methanol-chloroform from all these macromolecular fractions and analyzed for cholesterol, triglycerides, phospholipids. The fatty acid composition of the separated fractions was determined by GLC. The lipid composition and fatty acid spectrum of the macromolecular fractions of group I and group II aortas was compared. Total lipids increased in the freely extractable ("non associated lipids, approximately 78% of total) fraction as well as in the fraction "associated" with collagen and elastin. Free and esterified cholesterol increased also both in the "freely extractable" and in the collagen-elastin-associated lipids", approximately 78% of total) fraction as well was higher (+ 100%) than that of free cholesterol (+ 60%). Triglycerides increase also by 15 to 70% in all fractions except in the elastin-associated fraction. Free fatty acids increased by 40 to 400% in all extracts associated with macromolecular fractions but not in the "freely extractable" fraction where they decreased. Phospholipids show less marked variations (approximately less than 10%) and decrease in the elastin associated lipids of group II aortas. The fatty acid spectrum of group II lipids associated with macromolecules differs from that of group I. There is a relative increase of longer chains (C greater than 18, especially 20:1 and 20:2 acids). No such increase in the "long" fatty acids was seen in the "freely extractable" lipid fraction. Elastin isolated from group II aortas is significantly enriched in total lipids, cholesterol (free and esterified) and free fatty acids and contains the widest spectrum of fatty acids (from 11:2 to 22:1) with a significant fraction of total fatty acids as "odd" carbon chains. There appears to be a correlation between the decrease of triglyceride-bound fatty acids and the increase of free fatty acids. The free fatty acid concentration exceeds both in group I and II aortas the concentration of fatty acid esters. This increase in free fatty acids "associated" with intercellular matrix macromolecules and especially with elastin may be the result of an increased hydrolysis of esters and/or a decreased esterification in advanced atherosclerotic aortas. The accumulation of long chain and "odd" fatty acids in elastin may be an important factor in its accelerated degradation during the atherosclerotic process.
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