SPECIFIC ACCUMULATION OF LIPOPROTEIN(A) IN BALLOON-INJURED RABBIT AORTA IN-VIVO

Citation
Lb. Nielsen et al., SPECIFIC ACCUMULATION OF LIPOPROTEIN(A) IN BALLOON-INJURED RABBIT AORTA IN-VIVO, Circulation research, 78(4), 1996, pp. 615-626
Citations number
47
Categorie Soggetti
Hematology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
00097330
Volume
78
Issue
4
Year of publication
1996
Pages
615 - 626
Database
ISI
SICI code
0009-7330(1996)78:4<615:SAOLIB>2.0.ZU;2-3
Abstract
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.