Abstract We have investigated cytochemically the correlative distribution of lipoprotein (LP) components in successive lesional stages of plaque formation in hyperlipoproteinemic atherogenesis in the rabbit. Apoprotein B (apo B) was detected by an immunoperoxidase procedure, unesterified cholesterol (UC) by filipin and tomatine and phospholipid lamellae of the extracellular liposomes (EL) as they appear in standard EM. The changes were evaluated in relation to the state of endothelial cells and their transport pathways, and the reaction of the cellular and extracellular components of the intima. Each lesional stage has a relatively characteristic pattern distribution of the LP components. In fatty streaks with no endothelial denudation, apo B reaction product occurs mostly in non-particulate form associated with UC-rich EL; this suggests that transcytosed LP upon partial degradation and interaction with the extracellular components, reassemble as polymorphic EL-UC-apo B complexes. Serofibrinous insudates, although commonly devoid of EL and apo B, may contain UC presumably transported by a carrier other than LP. In advanced fibrolipidic lesions with open endothelial junctions and deendothelialized areas, a bulky intramural insudation of plasma results in the presence of large amounts of apparently little modified LP. This may represent what several investigators have isolated as “aortic LP”, which may be insudated rather than transported plasma LP.