弹性蛋白
腹主动脉瘤
动脉瘤
血管
灌注
医学
主动脉瘤
心脏病学
内科学
原弹性蛋白
解剖
肺
病理
炎症
主动脉破裂
钙化
血管疾病
腹部外科
循环系统
作者
Nozomu Ishikawa,Naoki Unno,Kazunori Inuzuka,Hajime Tsuyuki,Yusuke Endo,Yosuke Mihara,Kosuke Fukui,Masaki Sano,Kazuto Katahashi,Nobuhiro Zaima,Mayo Higashihara,Kazuya Yamada,Yoshiharu Matahira,Hiroya Takeuchi
标识
DOI:10.1038/s41598-026-57580-5
摘要
Abdominal aortic aneurysm (AAA) predominantly affects older individuals, yet the mechanisms by which aging increases susceptibility to aneurysm formation remain incompletely understood. The infrarenal aorta, where most AAAs develop, possesses sparse adventitial vasa vasorum (VV), suggesting limited mural perfusion reserve. We hypothesized that aging reduces the structural and biomechanical resilience of the aortic wall, thereby increasing vulnerability to hypoperfusion-induced degeneration. Using a previously established rat model of AAA induced by hypoperfusion of the adventitial VV, we compared young (12 weeks) and mature adult (24-28 weeks) rats exposed to identical hypoperfusion stress. At baseline, mature adult rats exhibited significantly lower aortic elastin content and reduced tensile strength compared with young rats, suggesting reduced structural reserve. Following hypoperfusion surgery, mature adult rats developed significantly larger aneurysms at postoperative Days 14 and 28 and showed a tendency toward increased rupture-related mortality. Histological analysis demonstrated more severe elastic fiber destruction in mature adult aneurysms. Although baseline VV patency tended to be lower in mature adult rats during aneurysm progression, aneurysm diameter showed an inverse correlation with elastin content. These findings suggest that baseline structural differences in the aortic wall may influence susceptibility to aneurysm formation under conditions of impaired mural perfusion. When considered together with the intrinsically sparse microvascular supply of the infrarenal aorta, these results are consistent with the concept that reduced elastin content and altered wall structure may enhance vulnerability to hypoperfusion-related degeneration. However, the mechanistic relationship between these factors cannot be determined from the present study.
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