To explore whether lipoprotein(a), Lp(a), may accumulate preferentiall
y to LDL in the arterial wall at sites of injury, cholesterol-fed rabb
its 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 l
abeled 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 t
wo lipoprotein fractions. In the second set of experiments, I-131-Lp(a
) (or I-131-LDL) was injected 26 hours before and I-125-Lp(a) (or I-12
5-LDL) 3 hours before the aorta was removed. Permeability and fraction
al 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 mu L/cm(2)
per hour versus 1.41+/-0.32 mu L/cm(2) per hour (nonpaired t test, P<.
0001); and fractional loss, 0.12+/-0.02 h(-1) versus 0.44+/-0.05 h(-1)
(non paired t test, P=.0001), respectively. Finally, after 23 hours'
exposure to labeled lipoproteins, the total accumulation and the amoun
t of tightly bound labeled Lp(a) in the balloon-injured intima-inner m
edia 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-i
njured compared with the normal aortic intima-inner media, the recover
y 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.