Specific accumulation of lipoprotein(a) in balloon-injured rabbit aorta in vivo.

To explore whether lipoprotein(a), Lp(a), may accumulate preferentially to LDL in the arterial wall at sites of injury, cholesterol-fed rabbits were injected intravenously with radiolabeled Lp(a) and/or LDL 3.1 +/- 0.1 days (mean +/- SEM, n = 30) after a balloon injury of the thoracic aorta. After 5 to 10 minutes' exposure to labeled lipoproteins, more labeled LDL than labeled Lp(a) was recovered in the intima-inner media of the balloon-injured segment (n = 9; paired t test, P < .0001); however, the amount of tightly bound labeled lipoprotein was similar for the two lipoprotein fractions. In the second set of experiments, 131I-Lp(a) (or 131I-LDL) was injected 26 hours before and 125I-Lp(a) (or 125I-LDL) 3 hours before the aorta was removed. Permeability and fractional loss of labeled Lp(a) (n = 8) versus LDL (n = 7) in the balloon-injured aortic intima-inner media were: permeability, 0.46 +/- 0.10 microL/cm2 per hour versus 1.41 +/- 0.32 microL/cm2 per hour (nonpaired t test, P < .0001); and fractional loss, 0.12 +/- 0.02 h-1 versus 0.44 +/- 0.05 h-1 (nonpaired t test, P = .0001), respectively. Finally, after 23 hours' exposure to labeled lipoproteins, the total accumulation and the amount of tightly bound labeled Lp(a) in the balloon-injured intima-inner media were, respectively, 174% (n = 6; ANOVA, P = .03) and 256% ANOVA, P = .005) of the values for labeled LDL. For labeled Lp(a) in the balloon-injured compared with the normal aortic intima-inner media, the recovery after 5 to 10 minutes, the permeability, and the accumulation after 23 hours were all increased, whereas the fractional loss was unchanged. These data suggest that the accumulation of Lp(a) is much larger in injured vessels than in normal vessels. Moreover, the data support the idea of a specific accumulation of Lp(a) compared with LDL in injured vessels.