Mehrabi Mohammad Reza, Huber Kurt, Serbecic Nermin, Wild Thomas, Wojta Johann, Tamaddon Forouzan, Morgan Abdelmonem, Ullrich Robert, Dietmar Glogar Helmut
Department of Cardiology, University of Vienna, Waehringer Guertel 18-20, Postfach 120, 1097, Vienna, Austria.
Thromb Res. 2002 Sep 1;107(5):189-96. doi: 10.1016/s0049-3848(02)00308-0.
In the present study, we sought to investigate whether elevated serum levels of homocysteine (Hcy), predisposing to endothelial dysfunction during progression of atherosclerosis, were paralleled by increased Hcy concentrations in human coronary arteries. Paraffin sections of coronary arteries were obtained from explanted hearts of cardiac transplant recipients suffering from coronary artery disease (CAD, n=32, mean age=56.6+/-6.8), and from heart donors where transplantation was not performed due to organization-related circumstances (Co, n=6, mean age 25.0+/-10.6), and characterized immunohistochemically for Hcy, CD68, and smooth muscle alpha-actin. Although the CAD group presented with high serum Hcy levels (27.7+/-12.8 micromol/l), the media and intimal layers containing the endothelium showed the lowest enrichment of Hcy (media: 20.8+/-4.4%; intima: 6.1+/-2.3%). Surprisingly, the control group revealed an extensive Hcy enrichment, co-localizing with vascular smooth cells (media: 32.3+/-14.0%; intima: 7.0+/-2.0%). In conclusion, we have provided evidence for a reverse relation between Hcy serum concentration and enrichment of Hcy in coronary arteries of patients with severe CAD, suggesting that Hcy is not likely to be involved directly in atheromatosis development of coronary arteries.
在本研究中,我们试图探究血清同型半胱氨酸(Hcy)水平升高(在动脉粥样硬化进展过程中易导致内皮功能障碍)是否与人类冠状动脉中Hcy浓度升高同时出现。冠状动脉石蜡切片取自患有冠状动脉疾病(CAD,n = 32,平均年龄 = 56.6±6.8)的心脏移植受者的离体心脏,以及因组织相关情况未进行移植的心脏供体(Co,n = 6,平均年龄25.0±10.6),并对其进行Hcy、CD68和平滑肌α-肌动蛋白的免疫组织化学特征分析。尽管CAD组血清Hcy水平较高(27.7±12.8微摩尔/升),但包含内皮的中膜和内膜层显示Hcy富集程度最低(中膜:20.8±4.4%;内膜:6.1±2.3%)。令人惊讶的是,对照组显示出广泛的Hcy富集,与血管平滑肌细胞共定位(中膜:32.3±14.0%;内膜:7.0±2.0%)。总之,我们提供了证据表明,严重CAD患者血清Hcy浓度与冠状动脉中Hcy富集之间呈反向关系,这表明Hcy不太可能直接参与冠状动脉粥样硬化的发展。