Atherosclerosic agents can promote the proliferation of smooth-muscle cells in the arterial intima (Stout, 1984). These cell colonies readily accumulate lipid, probably derived from plasma cholesterol and lipoproteins (Kramsch & Hollander, 1973). As the disease develops lipid deposits are also formed extracellularly and are retained in a loose network of connective tissue (Hajar et al., 1980). In the developed lesion, plaques, ulcerations and lipid-filled foam cells are characteristic features (Ross, 1981). The luminal surface of the aorta consists of a monolayer of endothelial cells, which covers a connective tissue containing smoothmuscle cells and elastic lamellae. Endothelial integrity is altered by the developing atheromatous lesion and permits entry to the connective tissue of plasma components that would normally be excluded. Access of elastase and plaque lipids could accelerate the degradation of the elastin component of the lamellae (Elliott & Darling, 1985). The lipid composition of the arteries from several species has been examined (Kramsch et al., 1971 ; Jacotot et al., 1973; Claire et al., 1976; Noma et al., 1979; Santillan et al., 1980). Chloroform/methanol (2 : 1, v/v) is the most commonly used solvent for the extraction of lipids (Folch et al., 1957). Homogenization is usually employed to obtain rapid quantitative extraction (Radin, 1969). An alternative lipid extraction process, using successive extractions of acetone and butan-1-01, has been used to de-lipidate elastin (Robert & Hornebeck, 1976). In the present work the aim was to remove the lipid from the aorta, yet avoid causing mechanical damage to the elastic lamellae. A lOcm segment of the thoracic aorta obtained during post-mortem examination had remaining adherent tissue removed with a scalpel before cutting into O.5cm wide bands. Twelve bands were washed in 0.9% (w/v) saline, at 4C, and half of the samples dehydrated to constant weight in a vacuum desiccator. The samples, six dehydrated (D) and six hydrated (H), were allocated to three extraction methods (A, B and C). Each method used 6 x 24h extractions at 4°C in closed and stirred containers. Method A : initial extraction was acetone followed by butan-1 -01. The sequence of acetone then butan1-01 was repeated twice, a total of six extractions. Material solubilized by extraction was recovered by removal of the solvent, with a rotary vacuum evaporator. Method B used chloroform/methanol (2 : I , v/v) under the same conditions as described in method A, and six extracts were recovered. Method C used a combination of methods A and B in the sequence acetone, butan-1-01. chloroform/methanol; this was repeated to give six extracts. The experiment produced a total of 36 lipid residues (Fig. I ) , each of which was solubilized in 3ml of chloroform for subsequent analysis. The total lipid in each extract was estimated by the phosphovanillan assay (Bauer, 1982). The lipid obtained from the aorta by the three extraction methods is shown in Fig. I(a). Lipid content has been expressed as a percentage of the initial wet weight of the tissue. The acetone/butan-I01 extraction yielded significantly less lipid than the chloroform/methanol extraction. There was no difference in lipid recovery between dehydrated and hydrated aorta samples, within the same extraction method. The quantity