In the development of atherosclerosis (AS), circulating monocytes emigrate into and accumulate in the intima as foamy cells. Interaction of the lipid laden macrophage (M phi) with cells of the arterial wall may contribute to the formation of atheromatous plaque. Using subcutaneous and peritoneal foamy cells (FC) collected from diet-induced hyperlipemia rabbits, the authors observed the influence of lipid laden on macrophage's functions relevant to AS lesion formation. In comparison with normal M phi, peritoneal FC were 4.8 and 5.4 fold more adhesive to the endothelial surface of intima preparation and the smooth muscle cells (SMC), while the adhesion rate produced by subcutaneous FC were increased 0.79 and 0.16 fold. SMC migration stimulated by both FC-conditioned medium slowed 5.78 and 5.90 fold increased respectively as in comparing with the control's, whereas normal M phi-conditioned medium only gave a 2.3 fold increase of SMC migration stimulation. In addition, both FC-conditioned medium stimulated SMC growth making 1.96 and 2.59 fold increase, and normal M phi-conditioned medium produced a 1.3 fold increase as compared with the control's. The results suggest that lipid-laden macrophages, may accelerate AS development due to changes of their biological properties. Since more than 95% of peritoneal macrophages as well as macrophages in the pleura, pericardial and synovial cavities from experimental hyperlipidemia rabbits are fully filled with lipid assuming the morphologic characteristics of atheromatous intimal foamy cells, it is considered that these cells will be valuable as the model.