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正常兔腹主动脉中低密度脂蛋白隔离的代谢证据。

Metabolic evidence for sequestration of low-density lipoprotein in abdominal aorta of normal rabbits.

作者信息

Schwenke D C

机构信息

Department of Pathology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1072, USA.

出版信息

Am J Physiol Heart Circ Physiol. 2000 Sep;279(3):H1128-40. doi: 10.1152/ajpheart.2000.279.3.H1128.

DOI:10.1152/ajpheart.2000.279.3.H1128
PMID:10993776
Abstract

In rabbits, atherosclerosis develops preferentially at branch sites compared with the adjacent uniform aorta. This study investigated the hypothesis that low-density lipoprotein (LDL) is "sequestered" (present in a form that exchanges slowly with plasma LDL) in the aortas of normal rabbits and that more LDL is sequestered at branch sites. Thus 33 normal rabbits were injected with LDL labeled with (125)I-labeled tyramine cellobiose ((125)I-TC) to trace both undegraded LDL and aortic LDL degradation products. For 25 rabbits, LDL was also labeled with (131)I to trace undegraded LDL alone. The time-dependent aortic (125)I-TC and (131)I accumulation was determined from 0.6 to 120 h after injection. Compartmental modeling provided metabolic evidence for sequestration of LDL at the branch (P < 0.01) and uniform (P < 0.005) abdominal aorta. Concentrations of sequestered LDL were 109 +/- 28% higher (P < 0.0005) for branch sites. LDL mean residence time was 23.5 +/- 3.1 h for branch sites, 7.6 +/- 3.5 h longer (P < 0.05) than for the uniform abdominal aorta. Enhanced retention of higher concentrations of sequestered LDL at branch sites could account for the increased susceptibility of these aortic sites to atherosclerosis.

摘要

与相邻的均匀主动脉相比,兔子的动脉粥样硬化优先在分支部位发展。本研究调查了以下假设:在正常兔子的主动脉中,低密度脂蛋白(LDL)被“隔离”(以与血浆LDL交换缓慢的形式存在),并且在分支部位有更多的LDL被隔离。因此,给33只正常兔子注射了用(125)I标记的纤维二糖酪胺((125)I-TC)标记的LDL,以追踪未降解的LDL和主动脉LDL降解产物。对于25只兔子,LDL还用(131)I标记,仅用于追踪未降解的LDL。在注射后0.6至120小时测定主动脉(125)I-TC和(131)I随时间的积累。房室模型提供了代谢证据,证明LDL在分支(P <0.01)和均匀(P <0.005)腹主动脉中被隔离。分支部位隔离的LDL浓度高109 +/- 28%(P <0.0005)。分支部位的LDL平均停留时间为23.5 +/- 3.1小时,比均匀腹主动脉长7.6 +/- 3.5小时(P <0.05)。分支部位更高浓度的隔离LDL的增强保留可能解释了这些主动脉部位对动脉粥样硬化易感性的增加。

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