Aarnoudse M W, Lamberts H B, Dijk F, Vos J, de Vries A J
Virchows Arch B Cell Pathol Incl Mol Pathol. 1984;47(3):211-6. doi: 10.1007/BF02890204.
Previous experiments have shown that local irradiation of the carotid arteries of hypercholesterolemic rabbits results in the development of atheromatosis in the irradiated areas of the arteries. The process starts with the adherence of monocytes to the endothelial layer, their entrance into the subendothelial space, and their subsequent transformation into lipophages (foam cells). Prevention of this type of plaque formation can be achieved by prednisolone (in a lower concentration than previously used) (Vos et al. 1981) and by VP16-213 (Vepesid). Differential blood cell counts demonstrated that the animals subjected to treatment with prednisolone developed a moderate relative lymphocytopenia, whereas treatment with Vepesid resulted in a severe monocytopenia. Since prednisolone treatment only partially prevented plaque formation, whereas Vepesid seemed to fully inhibit the development of plaques, we conclude that although a role of the lymphocyte in the process of plaque formation cannot be excluded, the monocyte seems to play a crucial role in the pathogenesis of radiation-induced atheromatosis.
先前的实验表明,对高胆固醇血症兔子的颈动脉进行局部照射会导致动脉照射区域出现动脉粥样硬化病变。这个过程始于单核细胞黏附于内皮细胞层,进入内皮下间隙,随后转变为脂肪吞噬细胞(泡沫细胞)。可以通过泼尼松龙(浓度低于先前使用的浓度)(沃斯等人,1981年)和依托泊苷(威猛)来预防这种类型的斑块形成。血细胞分类计数表明,接受泼尼松龙治疗的动物出现了中度相对淋巴细胞减少,而使用威猛治疗则导致严重的单核细胞减少。由于泼尼松龙治疗只能部分预防斑块形成,而威猛似乎能完全抑制斑块的发展,我们得出结论,虽然不能排除淋巴细胞在斑块形成过程中发挥作用,但单核细胞似乎在辐射诱导的动脉粥样硬化病变的发病机制中起关键作用。