Atherosclerotic lesions are most commonly found in big, high transmural pressure arteries, and are normally absent from veins (except when grafted into an arterial role) and from the pulmonary arteries (except under pulmonary hypertension). There have been a number of structural studies and tracer experiments that reveal differences between veins (~5 mmHg transmural pressure) and big arteries such as the aorta (~100 mmHg) and smaller ones such as the pulmonary artery (~16 mmHg). For example, Lever et al.'s (1990) study of albumin and Cr-EDTA uptake by different vessels' walls in rabbit indicated that the walls of the vena cava and the pulmonary artery have much greater void spaces for albumin than those of high-pressure systemic arteries such as the aorta and the carotid artery. Recently our group has shown that the hydraulic conductivity (Lp) of the intact inferior vena cava in rat is more than fifteen times larger and Lp of the pulmonary artery more than three times larger than Lp of the aorta. This indicates a logical consistency of a wall with a larger void space for water displaying a much smaller resistance to transmural water flow. In addition our group injected horseradish peroxidase (HRP) as a tracer into rats and, after sacrifice, examined their vessels en face in order to see how and where the tracer penetrated the tissue. In all three vessels HRP crossed the endothelium focally, rather than uniformly, but otherwise, the results in the vein were very different from those in the two arteries which, as noted last year, were surprisingly similar to each other. The early circulation time (~30 sec) spots in the vein were far larger than in either artery - the IVC the tracer spots are even larger at 30 seconds than that in the aorta at 4 minutes - yet they grew much more slowly. In previous studies we showed that similar two-dimensional filtration and convection-diffusion models could rationally explain the HRP spot growth in the aorta and the PA despite the different lumen pressures, hydraulic conductivities (or flow resistance), wall void and macromolecular diffusion coefficient in these vessels. In the present study, we use a 2D model similar in spirit, but with very different boundary conditions due to the different structure of vessel wall, e.g. the near absence of elastic sheets in the vein shown in TEM. In addition, Chuang et al. (1990) showed clusters of dead endothelial cells typically appeared in the IVC where HRP staining was concentrated, as opposed to single-cell leaks typical of the aorta and the PA. Our models show that these differences and the much larger Lp contribute to the significantly different growth of HRP spots. Solution of the mass transfer problem indicates vital differences in the tracer concentration profiles that may be relevant to the understanding of why veins have much lower susceptibilities to atherosclerosis than the large, high-pressure arteries.