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[外周血管和冠状动脉再狭窄病变中人类血管壁心肌细胞的体外运动性增加]

[Increased in vitro motility of human vascular wall myocytes from restenotic lesions of peripheral and coronary vessels].

作者信息

Bauriedel G, Windstetter U, Brandl R, Plas E, Kandolf R, Höfling B

机构信息

Medizinische Klinik I, Ludwig-Maximilians-Universität München.

出版信息

Z Kardiol. 1991 Aug;80(8):494-9.

PMID:1950071
Abstract

In this study we report on the successful cultivation of human peripheral and coronary plaque specimens selectively retrieved by percutaneous Simpson atherectomy and obtained by direct operative approach. A total of 32 patients in whom plaque tissue was excised from 22 primary and 10 restenotic lesions comprise the study population. Irrespective of their origin or location, all advanced lesions showed smooth muscle cells (SMC) to be their predominant cell type proven by indirect immunofluorescence technique. Cultured endothelial cells were only identified in 2/6 surgically removed samples. Locomotion analysis of cultured smooth muscle cells was performed with a standardized computer-assisted video system. Cells of all groups exhibited random motility. However, SMC migratory velocity of restenotic origin amounted to 47.4 +/- 3.4 microns/h (n = 10, x +/- SD) and thereby was found 2.4 times (p less than 0.001) increased as compared to primary lesion values of 22.0 +/- 3.7 microns/h (n = 22, x +/- SD). This highly significant difference was seen for both peripheral and coronary lesions. Our data suggest increased SMC migratory activity to represent a basic biological mechanism involved in human accelerated arteriosclerosis and restenosis formation.

摘要

在本研究中,我们报告了通过经皮辛普森旋切术选择性获取并经直接手术方法获得的人类外周和冠状动脉斑块标本的成功培养情况。共有32例患者,其斑块组织取自22个原发性病变和10个再狭窄病变,构成了研究人群。无论其起源或位置如何,所有晚期病变经间接免疫荧光技术证实,平滑肌细胞(SMC)是其主要细胞类型。仅在2/6个手术切除样本中鉴定出培养的内皮细胞。使用标准化的计算机辅助视频系统对培养的平滑肌细胞进行运动分析。所有组的细胞均表现出随机运动。然而,再狭窄来源的SMC迁移速度为47.4±3.4微米/小时(n = 10,x±SD),因此与原发性病变值22.0±3.7微米/小时(n = 22,x±SD)相比,发现增加了2.4倍(p <0.001)。外周和冠状动脉病变均出现这种高度显著差异。我们的数据表明,SMC迁移活性增加代表了人类加速动脉粥样硬化和再狭窄形成所涉及的一种基本生物学机制。

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1
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Z Kardiol. 1991 Aug;80(8):494-9.
2
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