Morrel E M, Holland J A, Pritchard K A, Colton C K, Stemerman M B
Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge 02139.
Ann N Y Acad Sci. 1987;516:412-7. doi: 10.1111/j.1749-6632.1987.tb33060.x.
The focal entry and accumulation of LDL within the arterial wall of the normal animal may represent an early stage in the development of the atherosclerotic plaque. Concentrations of LDL 10 to 100 times normal medial concentrations might be difficult to clear from the arterial wall, permitting accumulation of lipid. Elevated LDL concentrations, in proximity to smooth muscle cells, appear to stimulate SMC proliferation. High LDL concentrations might also enhance mononuclear cell adhesion to endothelium. Since LDL has a high affinity for heparin and heparin for growth factors, LDL accumulation may be a mechanism for the concentration of such materials in the intima. The observation of markedly enhanced macromolecular permeability foci could be related to several potential mechanisms of initiation of atherosclerosis. This observation is of particular note when the focal occurrence of atherosclerosis is considered. Although atherosclerosis is seen as a generalized thickening of the intima, it is the focal narrowing of the lumen that is often responsible for the stenosis which produces symptoms such as angina or myocardial infarction.
在正常动物的动脉壁中，低密度脂蛋白（LDL）的局灶性进入和聚集可能代表动脉粥样硬化斑块形成的早期阶段。动脉壁中LDL的浓度比正常中膜浓度高10到100倍，可能难以从动脉壁清除，从而导致脂质积聚。靠近平滑肌细胞的LDL浓度升高似乎会刺激平滑肌细胞增殖。高LDL浓度还可能增强单核细胞与内皮的粘附。由于LDL对肝素具有高亲和力，而肝素对生长因子具有高亲和力，LDL积聚可能是这些物质在内膜中浓缩的一种机制。大分子通透性灶明显增强的观察结果可能与动脉粥样硬化起始的几种潜在机制有关。当考虑动脉粥样硬化的局灶性发生时，这一观察结果尤为值得注意。尽管动脉粥样硬化被视为内膜的普遍性增厚，但往往是管腔的局灶性狭窄导致了诸如心绞痛或心肌梗死等症状的狭窄。
