White J V, Haas K, Phillips S, Comerota A J
Frederick A. Reichle Surgical Research Laboratory, Temple University Medical School, Philadelphia, PA 19140.
J Vasc Surg. 1993 Feb;17(2):371-80; discussion 380-1. doi: 10.1067/mva.1993.43023.
Adventitial elastin degradation is a hallmark of abdominal aortic aneurysm (AAA) formation in human beings, although the quantitative relationship between elastin loss and AAA formation and growth is unknown. This study was undertaken to quantitate the reduction of adventitial elastin for small AAA, to determine whether the loss of this structural component parallels aneurysm growth, and to examine the ultrastructure of the remaining elastin elements.
Longitudinal strips of anterior aneurysm wall were taken from 12 patients having elective repair of small (diameter < 5 cm, n = 4), moderate (diameter < 5 to 7 cm, n = 4), or large (diameter > 7 cm, n = 4) AAA and from six normal control subjects at autopsy. Specimens were prepared with elastin and collagen stains for histologic examination or formic acid for scanning electron microscopic evaluation of elastin architecture. Adventitial elastin content of aneurysmal and control aortas was quantitated with video microscopy and compared by aneurysm diameter.
The inner portion of adventitia of normal aortic wall was composed of densely compacted alternating lamellae of elastin and collagen, which were grossly disrupted in all aneurysms. The remaining elastin fibers were disorganized and tortuous. There was an 81.6% +/- 2.1% reduction in elastin lamellae and an 85.7% +/- 4.2% reduction in fibers per lamellae compared with the number in control aortas (p < 0.001). Size of the aneurysm made no difference in adventitial elastin content.
These data strongly suggest that elastolysis is a primary event in AAA formation that occurs before over loss of adventitial structural integrity and the development of small aneurysms.
外膜弹性蛋白降解是人类腹主动脉瘤（AAA）形成的一个标志，尽管弹性蛋白丢失与AAA形成和生长之间的定量关系尚不清楚。本研究旨在定量小AAA中外膜弹性蛋白的减少情况，确定这种结构成分的丢失是否与动脉瘤生长平行，并检查剩余弹性蛋白成分的超微结构。
从12例行择期修复的小（直径<5 cm，n = 4）、中（直径5至7 cm，n = 4）或大（直径>7 cm，n = 4）AAA患者以及6名正常对照受试者的尸检主动脉中获取动脉瘤前壁的纵向条带。标本用弹性蛋白和胶原染色进行组织学检查，或用甲酸进行弹性蛋白结构的扫描电子显微镜评估。通过视频显微镜对动脉瘤和对照主动脉的外膜弹性蛋白含量进行定量，并按动脉瘤直径进行比较。
正常主动脉壁外膜的内层由紧密压实的弹性蛋白和胶原交替薄片组成，在所有动脉瘤中均严重破坏。剩余的弹性纤维杂乱且弯曲。与对照主动脉相比，弹性蛋白薄片减少了81.6%±2.1%，每层纤维减少了85.7%±4.2%（p<0.001）。动脉瘤大小对外膜弹性蛋白含量无影响。
这些数据强烈表明，弹性蛋白溶解是AAA形成中的一个主要事件，发生在外膜结构完整性过度丧失和小动脉瘤发展之前。
