Nielsen L B, Stender S, Kjeldsen K, Nordestgaard B G
Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Denmark.
Circ Res. 1996 Apr;78(4):615-26. doi: 10.1161/01.res.78.4.615.
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.
为探究脂蛋白(a) [Lp(a)]在动脉壁损伤部位是否比低密度脂蛋白(LDL)更易优先蓄积，给喂食胆固醇的家兔在胸主动脉球囊损伤后3.1±0.1天（均值±标准误，n = 30）经静脉注射放射性标记的Lp(a)和/或LDL。在与标记脂蛋白接触5至10分钟后，在球囊损伤节段的内膜-内中膜中回收的标记LDL比标记Lp(a)更多（n = 9；配对t检验，P <.0001）；然而，两个脂蛋白组分紧密结合的标记脂蛋白量相似。在第二组实验中，在移除主动脉前26小时注射131I-Lp(a)（或131I-LDL），3小时前注射125I-Lp(a)（或125I-LDL）。球囊损伤的主动脉内膜-内中膜中标记Lp(a)（n = 8）与LDL（n = 7）的通透性和分数丢失分别为：通透性，0.46±0.10微升/平方厘米·小时对1.41±0.32微升/平方厘米·小时（非配对t检验，P <.0001）；分数丢失，0.12±0.02小时-1对0.44±0.05小时-1（非配对t检验，P =.0001）。最后，在与标记脂蛋白接触23小时后，球囊损伤的内膜-内中膜中标记Lp(a)的总蓄积量和紧密结合量分别为标记LDL值的174%（n = 6；方差分析，P =.03）和256%（方差分析，P =.005）。与正常主动脉内膜-内中膜相比，球囊损伤处标记Lp(a)在5至10分钟后的回收率、通透性以及23小时后的蓄积量均增加，而分数丢失不变。这些数据表明，Lp(a)在损伤血管中的蓄积比在正常血管中要大得多。此外，数据支持Lp(a)在损伤血管中与LDL相比存在特异性蓄积的观点。
