Early atherosclerosis is accompanied by a decreased rather than an increased accumulation of fatty acid hydroxyderivatives.

The content of 13-hydroxylinoleic acid (13-HODE) and 15-hydroxyarachidonic acid (15-HETE) in the rabbit thoracic aorta was measured using high performance liquid chromatography after chronic exposure to cholesterol and a high dose of molsidomine, a donor of nitric oxide (NO). Cholesterol-induced fatty streak formation was accompanied by a decrease in the amounts of esterified 13-HODE and 15-HETE. The reduction of the esterified 13-HODE content correlated significantly with the severity of the lesions. These results do not support the hypothesis that fatty acid hydroperoxides accumulate in the arterial wall during atherosclerosis. On the other hand, the quantity of esterified 13-HODE and 15-HETE was increased markedly after exposure to molsidomine. The high dose of this agent could have initiated radical reactions (via liberation of NO and production of superoxide anions) thereby leading to a raise of the 13-HODE and 15-HETE content of the vessel.