Popov A V, Ketlinski S A, Tararak E M
Paroi Arterielle. 1975 Dec;3(2):61-9.
Historadioautographic and biochemical studies were undertaken on the transport of 14C-labelled serum very low density and low density lipoproteins (VLDL and LDL respectively) into the aortic wall. Aortas from normal and atherosclerotic rabbits were perfused in vitro with a medium containing VLDL and LDL for 6 hours. Historadioautography revealed the label in all the layers of the perfused aorta. The gradient in the distribution of this label from the inner layers of the aortic wall dawn to the outer part of the media demonstrated that lipoprotein infiltration of the vessel wall is due to uptake of lipoproteins from the aortic lumen. The non-uniform pattern of the distribution of lipoproteins taken up by the atherosclerotic aorta was considered as a result of atherogenesis induced changes in the aortic connective tissue. Both morphological and biochemical studies revealed the increased permeability of the atherosclerotic aortic wall to VLDL and LDL, which appeared to penetrate the walls of blood vessels in the form of intact particles.
进行了放射性自显影和生化研究，以探讨14C标记的血清极低密度脂蛋白和低密度脂蛋白（分别为VLDL和LDL）向主动脉壁的转运。用含有VLDL和LDL的培养基对正常和动脉粥样硬化兔子的主动脉进行体外灌注6小时。放射性自显影显示灌注主动脉的所有层均有标记。该标记物从主动脉壁内层到中膜外层的分布梯度表明，血管壁的脂蛋白浸润是由于从主动脉腔摄取脂蛋白所致。动脉粥样硬化主动脉摄取的脂蛋白分布不均匀模式被认为是动脉粥样硬化发生导致主动脉结缔组织变化的结果。形态学和生化研究均显示，动脉粥样硬化主动脉壁对VLDL和LDL的通透性增加，这些脂蛋白似乎以完整颗粒的形式穿透血管壁。
