Origuchi N, Shigematsu H, Izumiyama N, Nakamura K, Toku A, Muto T
First Department of Surgery, Faculty of Medicine, The University of Tokyo, Japan.
Int Angiol. 1998 Jun;17(2):113-9.
The pathogenesis of aortic aneurysms remains largely unknown, despite aneurysmal rupture being an increasingly common catastrophe.
This study was designed to elucidate the mechanism of arterial dilatation histologically and electron microscopically, utilising a new animal model. Elastase, 3.0 mg/ml, was applied to the abdominal aortae of 18 New Zealand white rabbits from the adventitia side for 3 hours. The rabbits were sacrificed at 0, 3, 14, 28, 42 and 90 days after the procedure (n=4, 3, 2, 2, 2, 3).
Two rabbits were found to have developed aortic rupture. On day 0, elastase application induced fusiform aneurysms up to 1.62+/-0.14 times the pre-elastase application aortic diameter. Dilated walls revealed medial elastolysis, degeneration of smooth muscle cells (SMCs) and damaged endothelial cells. By day 3, the smooth muscle cells had changed to the synthetic type. Aneurysms did not progress, and after 42 days, showed gradual shrinkage. By day 90, aortic diameters had nearly normalised.
Aortic walls also returned to the pre-elastase application thickness and some mature medial elastic lamellae showed regeneration. Medial smooth muscle cells reverted to the contractile type. Aortic dilatation induced by peri-aortic application of elastase heals spontaneously, accompanied by regeneration of smooth muscle cells. Irreversible degeneration of medial smooth muscle cells appears to be more critical to aneurysm formation than degeneration of elastic lamellae.
尽管动脉瘤破裂是一种日益常见的灾难性事件，但主动脉瘤的发病机制在很大程度上仍不清楚。
本研究旨在利用一种新的动物模型，从组织学和电子显微镜角度阐明动脉扩张的机制。将3.0mg/ml的弹性蛋白酶从外膜侧施加到18只新西兰白兔的腹主动脉上，持续3小时。在手术后0、3、14、28、42和90天处死兔子（每组分别为n = 4、3、2、2、2、3只）。
发现两只兔子发生了主动脉破裂。在第0天，应用弹性蛋白酶诱发梭形动脉瘤，其直径达到应用弹性蛋白酶前主动脉直径的1.62±0.14倍。扩张的血管壁显示中层弹性纤维溶解、平滑肌细胞（SMC）变性和内皮细胞受损。到第3天，平滑肌细胞已转变为合成型。动脉瘤没有进展，42天后逐渐缩小。到第90天，主动脉直径几乎恢复正常。
主动脉壁也恢复到应用弹性蛋白酶前的厚度，一些成熟的中层弹性膜显示出再生。中层平滑肌细胞恢复为收缩型。主动脉周围应用弹性蛋白酶诱导的主动脉扩张可自发愈合，伴有平滑肌细胞再生。中层平滑肌细胞的不可逆变性似乎比弹性膜变性对动脉瘤形成更为关键。
