THE ENDOTHELIUM OF ADVANCED ARTERIOSCLEROTIC PLAQUES IN HUMANS
THE ENDOTHELIUM OF ADVANCED ARTERIOSCLEROTIC PLAQUES IN HUMANS
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DOI：
10.1161/01.atv.11.6.1678
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发表时间：
1991-11-01
期刊：
影响因子：
--
通讯作者：
BURRIG, KF
中科院分区：
文献类型：
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作者：
BURRIG, KF
在颈动脉内膜切除术标本和因晚期缺血性心脏病而移植的心脏的冠状动脉中，研究了覆盖晚期但不复杂的人类硬化斑块的内皮细胞的功能形态。内皮层几乎总是完好无损的，内皮图样反映了预期的狭窄动脉的局部血流模式，其中大部分是狭窄下游的血流异常。斑块表面常可见大(巨型)内皮细胞(定义为表面积大于或等于800mU-m2的内皮细胞)，这可能表明内皮细胞的加速衰老可归因于受扰血流区域持续的非剥脱损伤。超微结构上，内皮细胞激活频繁，细胞器增生。此外，作为免疫激活的标志，约5%的内皮细胞表达II类抗原(HLA-DR和罕见的局灶性HLA-DQ)，通过与von Willebrand因子的双重免疫荧光来鉴定内皮细胞。EC的激活可能是激活的血小板和单核细胞黏附于完整的管腔表面的原因，这些细胞总是存在的(与非硬化性动脉段相反)。此外，肌内皮细胞与内皮下修饰的平滑肌细胞的接触增加是硬化性病变的正常特征；这一特征代表了硬化性病变中EC与平滑肌细胞相互作用的未知过程，可能是EC控制平滑肌细胞增殖的代偿过程。在晚期斑块中，内皮细胞在没有剥蚀的情况下发生改变，但性质发生了变化，这可能有助于斑块的生长，这与动脉硬化性病变发病机制中的内皮细胞功能障碍是一致的。
The functional morphology of the endothelial cells (ECs) covering advanced but uncomplicated sclerotic plaques in humans was studied in carotid endarterectomy specimens and in coronary arteries from hearts explanted because of advanced ischemic heart disease. The endothelial layer was nearly always intact, and the endothelial patterns reflected the anticipated local flow patterns along the narrowed arteries, with the majority of flow irregularities downstream from the stenosis. Large (giant) ECs (defined as ECs with a surface area of greater-than-or-equal-to 800-mu-m2) were frequently found on the plaque surface, probably indicating accelerated EC senescence attributable to sustained nondenuding injury in the region of disturbed flow. Ultrastructurally, activation of ECs with hyperplasia of organelles was frequent. In addition, as a sign of immunological activation, about 5% of ECs express class II antigens (HLA-DR and rarely focal HLA-DQ), as demonstrated by double immunofluorescence with von Willebrand factor to identify the ECs. EC activation may be responsible for adherence to the intact luminal surface by activated platelets and monocytes, which were always present (in contrast with nonsclerotic artery segments). Furthermore, an increase in myo-endothelial contacts to subendothelial modified smooth muscel cells was a regular feature of the sclerotic lesions; this feature represents an unknown process of EC and smooth muscle cell interaction in the sclerotic lesion and may be a compensatory process for EC control of smooth muscle cell proliferation. In advanced plaques the ECs are altered without denudation but with changed properties, which may contribute to plaque growth and which are consistent with the postulated EC dysfunction in the pathogenesis of arteriosclerotic lesions.