Adhesion of platelets to the arterial subendothelium exposed by injury to the endothelium, is thought to initiate atherosclerosis. Thermodynamically, adhesion will occur if it decreases the free energy of the system. Here, I have developed a contact angle technique to measure relative changes in the interfacial free energy of the arterial wall, before and after removal of the endothelium. Sections of aorta were tested with an equilibrium two phase system of 4% poly (ethylene glycol) (PEG)/4% dextran, in buffered physiological saline. The tissue was immersed in the PEG phase and droplets of the denser dextran phase were placed on its lumenal surface. After testing, the endothelium was removed with a saline jet, and the tissue was retested. Contact angles of 86.0 (+OR-) 1.1(DEGREES) (SEM), n = 64 for the intact endothelium, and 20.0 (+OR-) 0.08 (SEM), n = 61 on the subendothelium, were measured from photomicrographs. Since the physical behavior of blood is similar to the PEG phase, the subendothelium probably represents a high energy surface in vivo, thus promoting platelet adhesion.;Factors which cause endothelial injury may act chronically at the cell surface to cause desquamation. To test this hypothesis, rabbits fed a 2% cholesterol diet to induce atherosclerosis were divided into 3 experimental groups: continuous feeding, interrupted feeding, and controls. Areas proximal and distal to intercostal orifices, where no plaque had yet developed, were tested with the PEG/dextran system. Proximal areas on the diseased arteries, and both the proximal and distal locations in controls gave contact angles of approximately 90(DEGREES); however those areas distal to orifices, where lesions eventually occur, yielded significantly different angles, 78(DEGREES). This difference indicates a change in the glycocalyx, which could weaken the cell resistance to injury, leading to desquamation, platelet adhesion and plaque formation
