Effects of injury on apoB kinetics and concentration in rabbit aorta.

Endothelial injury or dysfunction and deposition of lipoproteins and cholesterol are key events during the development of atherosclerosis. We have studied the lipoprotein kinetics in arterial tissue in relation to endothelial injury and re-endothelialization. Endothelial injury was induced in rabbits by use of a balloon catheter. With a specific immunoradiometric assay, apoB levels in arterial tissue were measured at different time points for up to 10 weeks after injury. Forty-five minutes before being killed, the rabbits were injected with 125I-LDL, and influx of LDL was calculated from the accumulation of radioactivity in the arterial tissue. The concentration of apoB in the injured arterial tissue was four times higher than that in control arterial tissue (P < .0001). Within the lesion the concentration was as high in nonendothelialized as in re-endothelialized regions. The tissue pool of apoB was divided into a loosely bound fraction and a tightly bound fraction. The increase of apoB in the injured areas was primarily due to an increase in the tightly bound fraction. The influx of apoB was severalfold higher in nonendothelialized tissue than in re-endothelialized tissue or control areas (P < .005). When retention time was calculated, this was found to dramatically increase (by seven times) the tightly bound pool of apoB in the re-endothelialized areas. In addition to the large increase of a tightly bound apoB pool in injured areas, we found a prolonged retention time of apoB in the lesions, but only in the re-endothelialized areas.(ABSTRACT TRUNCATED AT 250 WORDS)