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We previously showed by qualitative en face autoradiography that after 24 hours of circulation, 125I-labeled low density lipoprotein (LDL) injected in tracer amounts accumulated focally at the edges of regenerating endothelial islands in the balloon catheter-deendothelialized aorta of the normocholesterolemic rabbit. In the present study with the same animal model, we have used quantitative autoradiography to examine 125I-LDL accumulation in the healing aorta as a function of LDL circulation time from 2.5 to 40 hours. The results demonstrated that 125I-LDL accumulation in the healing aorta occurred in two kinetically and biochemically distinct compartments, one of which was in equilibrium with plasma and one of which sequestered LDL. LDL accumulation in the still-deendothelialized aorta (DEA) was diffuse and only moderately intense on autoradiography. It peaked 4 hours after injection; over the following 36 hours the disappearance of 125I-LDL from DEA paralleled the disappearance of 125I-LDL from plasma. In contrast, accumulation of 125I-LDL at the edges of regenerating endothelial islands was focal and intense. LDL accumulation in this compartment also peaked 4 hours after injection but remained elevated even at 40 hours, despite falling plasma levels of LDL. At 24 hours, edge LDL accumulation per unit area was more than five times greater than DEA accumulation. The data indicate that LDL accumulation in specific compartments of the functionally modified arterial wall occurs independently of either acute or chronic hypercholesterolemia. The contrast between labile LDL accumulation in DEA and persistent accumulation at the edges of healing aortic islands indicates that LDL accumulation in the two areas must involve different processes within the arterial wall itself.

Time course of 125I-labeled LDL accumulation in the healing, balloon-deendothelialized rabbit aorta.