Andrews E J, White W J, Bullock L P
Am J Pathol. 1975 Feb;78(2):199-210.
The pathogenesis of aneurysm formation was studied in Blotchy (Blo) mice which have a hereditary defect in collagen and elastin cross-linking. Elastin breakdown began at an early age and progressed rapidly. Changes observed included replacement of elastica by fibroblasts and ground substance. More advanced lesions were characterized by infiltrates of inflammatory cells, hemorrhages, and eventual ruptures of the aortic wall. Accumulations of lipids, Schiff-positive mucopolysaccharides, iron or calcium were not found. The lesions occurred primarily at points of greatest stress and were confined to the thoracic aorta. Androgen-insensitive mice (Tfm/Y) with the Blo gene died at a significantly earlier age than did normal Blo males or Blo/plus females. The Blo mouse is compared with other animal models of spontaneous and experimentally produced aneurysms.
在斑点（Blo）小鼠中研究了动脉瘤形成的发病机制，这些小鼠在胶原蛋白和弹性蛋白交联方面存在遗传性缺陷。弹性蛋白分解在幼年时开始并迅速进展。观察到的变化包括成纤维细胞和基质替代弹性组织。更晚期的病变特征为炎性细胞浸润、出血以及主动脉壁最终破裂。未发现脂质、席夫阳性粘多糖、铁或钙的积聚。病变主要发生在应力最大的部位，且局限于胸主动脉。携带Blo基因的雄激素不敏感小鼠（Tfm/Y）比正常的Blo雄性小鼠或Blo/杂合雌性小鼠死亡年龄显著更早。将Blo小鼠与其他自发性和实验性动脉瘤动物模型进行了比较。
