Selective increase in cholesterol at atherosclerosis-susceptible aortic sites after short-term cholesterol feeding.
Selective increase in cholesterol at atherosclerosis-susceptible aortic sites after short-term cholesterol feeding.
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短期胆固醇喂养后，动脉粥样硬化易感主动脉部位的胆固醇选择性增加。
DOI：
10.1161/01.atv.15.11.1928
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Schwenke,DC
中科院分区：
文献类型：
--
作者：
Schwenke,DC
在家兔中，主动脉弓和降胸及腹主动脉的分支部位易发生动脉粥样硬化。本研究调查了以下假设：在喂食胆固醇4至8天后，报告的LDL浓度和敏感主动脉部位平均停留时间的局灶性增加先于动脉粥样硬化变化，如主动脉胆固醇浓度增加所示。正常家兔主动脉各部位的胆固醇浓度相似（约2.8 μmol/g）。喂食胆固醇8天后，未检测到主动脉胆固醇浓度的变化。然而，在喂食胆固醇12和16天后，与正常家兔的腹分支部位相比，腹分支部位的胆固醇浓度升高（分别为4.47±0.50，n=8和4.85±0.33，n=11，μmol/g对2.87±0.27，n=12，μmol/g;分别为P<0.025和P <0.005）。相反，动脉粥样硬化抵抗的非分支腹主动脉的胆固醇浓度在喂食胆固醇16天后没有变化，并且远低于分支部位的胆固醇浓度（2.72±0.12对4.85±0.33 μmol/g，n=11;P<0.001）。其他敏感部位的胆固醇浓度也在喂食胆固醇12天和16天后增加。敏感部位的胆固醇浓度与高胆固醇血症的持续时间和程度呈线性相关（P<0.001至P <0.0001），而耐药部位则没有这种关系。喂食胆固醇12天和16天后，大部分（59%至93%）胆固醇在敏感主动脉部位积聚，未酯化，表明胆固醇浓度增加并不反映泡沫细胞的发育或血浆脂蛋白的渗出。这项研究表明，报告的局灶性增加低密度脂蛋白浓度和平均停留时间在敏感的主动脉部位在胆固醇喂养动脉粥样硬化之前。
In rabbits, the aortic arch and branch sites of the descending thoracic and abdominal aortas are susceptible to atherosclerosis. This study investigated the hypothesis that the reported focal increase in LDL concentration and mean residence time at susceptible aortic sites after feeding cholesterol for 4 to 8 days precede atherosclerotic change as indicated by increased aortic cholesterol concentration. Cholesterol concentrations for all aortic sites of normal rabbits were similar (≈2.8 μmol/g). No change in aortic cholesterol concentration could be detected after feeding cholesterol for 8 days. However, after feeding cholesterol for 12 and 16 days, cholesterol concentrations for abdominal branch sites were increased compared with abdominal branch sites of normal rabbits (4.47±0.50, n=8, and 4.85±0.33, n=11, μmol/g, respectively, versus 2.87±0.27, n=12, μmol/g;P<.025 andP<.005, respectively). In contrast, the cholesterol concentration of atherosclerosis-resistant nonbranch abdominal aorta was unchanged after feeding cholesterol for 16 days and was much less than that of the branch sites (2.72±0.12 versus 4.85±0.33 μmol/g, n=11;P<.001). Cholesterol concentrations for other susceptible sites were also increased after feeding cholesterol for 12 and 16 days. Cholesterol concentrations for susceptible sites were linearly related to a combined measure of duration and extent of hypercholesterolemia (P<.001 toP<.0001), whereas no such relationship could be detected for resistant sites. Most (59% to 93%) of the cholesterol accumulating in susceptible aortic sites after feeding cholesterol for 12 and 16 days was nonesterified, suggesting that the increased cholesterol concentration did not reflect development of foam cells or the insudation of plasma lipoproteins. This study suggests that the reported focal increases in LDL concentration and mean residence time at susceptible aortic sites during cholesterol feeding precede atherosclerosis.