Tanasković Irena, Mladenović-Mihailović Aleksandra, Usaj-Knezević Slavica, Stanković Vesna, Aleksić Aleksandar, Kastratović Tatjana, Aleksić Aleksandra, Lazić Zorica, Mladenović-Bogdanović Zorica, Zivanović Aleksandar, Djurić Janko, Jovicić Ugljesa, Sorak Marija
Medicinski fakultetu Kragujevac, Katedra za histologiju i embriologiju, Kragujevac, Srbija.
Vojnosanit Pregl. 2010 Dec;67(12):959-64. doi: 10.2298/vsp1012959t.
BACKGROUND/AIM: The main complication of the atherosclerotic abdominal aortic aneurysm (AAA) is her rupture that begins with lesion in intima and rupture. The purpose of this work was to determine immunocytochemical and morphofunctional characteristics of the cells in aortic wall in ruptured atherosclerotic abdominal aortic aneurysm.
During the course of this study, 20 samples of atherosclerotic AAA were analyzed, all of them obtained during authopsy. The samples were fixed in 4% formalin and embedded in paraffin. Sections of 5 microm thickness were stained histochemically (of Heidenhain azan stain and Periodic acid Schiff--PAS stain) and immunocytochemically using a DAKO LSAB+/HRP technique to identify alpha-smooth muscle actin (alpha-SMA), vimentin, myosin heavy chains (MHC), desmin, S-100 protein, CD45 and CD68 (DAKO specification).
The results of our study showed that ruptured atherosclerotic AAA is characterized by a complete absence of endothelial cells, the disruption of basal membrane and internal elastic lamina, as well as a presence of the remains of hypocellular complicated atherosclerotic lesion in intima. On the plaque margins, as well as in the media, smooth muscle cells (SMCs) are present, which express a alpha-SMA and vimentin (but without MHC or desmin expression), as well as leukocyte infiltration, and a large number of foam cells. Some of the foam cells show a CD68- immunoreactivity, while the others show vimentin- and S-100 protein-immunoreactivity. Media is thinned out with a disorganized elastic lamellas, while adventitia is characterized by inflammatory inflitrate (infection).
Rupture of aneurysm occurs from the primary intimal disruption, which spreads into thinned out media and adventitia. Rupture is caused by unstable atherom, hypocellularity, loss of contractile characteristics of smooth muscle cells in intima and media, neovascularization of the media, as well as by the activity of the macrophages in the lesion.
背景/目的：动脉粥样硬化性腹主动脉瘤（AAA）的主要并发症是破裂，其始于内膜病变和破裂。本研究的目的是确定破裂的动脉粥样硬化性腹主动脉瘤主动脉壁细胞的免疫细胞化学和形态功能特征。
在本研究过程中，分析了20例动脉粥样硬化性AAA样本，均取自尸检。样本用4%福尔马林固定并石蜡包埋。5微米厚的切片进行组织化学染色（海登海因偶氮染色和过碘酸希夫染色-PAS染色），并使用DAKO LSAB+/HRP技术进行免疫细胞化学染色，以鉴定α-平滑肌肌动蛋白（α-SMA）、波形蛋白、肌球蛋白重链（MHC）、结蛋白、S-100蛋白、CD45和CD68（DAKO说明书）。
我们的研究结果表明，破裂的动脉粥样硬化性AAA的特征是内皮细胞完全缺失、基底膜和内弹性膜破坏，以及内膜中存在细胞减少的复杂动脉粥样硬化病变遗迹。在斑块边缘以及中膜中，存在平滑肌细胞（SMC），其表达α-SMA和波形蛋白（但不表达MHC或结蛋白），以及白细胞浸润和大量泡沫细胞。一些泡沫细胞显示CD68免疫反应性，而其他泡沫细胞显示波形蛋白和S-100蛋白免疫反应性。中膜变薄，弹性板排列紊乱，而外膜的特征是炎症浸润（感染）。
动脉瘤破裂源于原发性内膜破坏，其扩展至变薄的中膜和外膜。破裂是由不稳定的动脉粥样硬化、细胞减少、内膜和中膜平滑肌细胞收缩特性丧失、中膜新生血管形成以及病变中巨噬细胞的活性引起的。
