Experimental aortic intimal thickening has been induced in rabbits by two types of injury, suture placement and electrocautery. Scanning electron microscopy showed that endothelialization of the suture plaque was completed at about 10 days following injury. New endothelial cells had no particular orientation or were oriented at right angles to the adjacent normal aortic endothelium. Realignment parallel with the aortic axis had occurred by 21 days after induction of the lesion. Orientation patterns of new endothelial cells over irregularly shaped cautery-induced intimal thickening were difficult to ascertain. Aortic permeability studies were accomplished by using the tracers horseradish peroxidase (HRP) and ferritin. Several naturally occurring intimal thickenings in normal aortas had greater permeability for HRP than did adjacent normal intima. An enhanced penetration of both tracers was observed in mature intimal lesions produced by both experimental procedures compared to adjacent morphologically normal aortic intima. HRP molecules entered the thickened aortic intima in increased amounts through interendothelial junctions and by endothelial pinocytotic vesicles; ferritin molecules were seen only in pinocytotic vesicles. Increased penetration of HRP was observed for as long as 27 weeks after injury, while that of ferritin was observed only for 3 weeks. The enhanced permeability of the thickened intima as compared to normal for these two tracers of considerably different sizes strongly suggests an increased permeability of endothelium overlying intimal thickening for naturally circulating macromolecules.