Tanaka Hiroki, Zaima Nobuhiro, Sasaki Takeshi, Sano Masaki, Yamamoto Naoto, Saito Takaaki, Inuzuka Kazunori, Hayasaka Takahiro, Goto-Inoue Naoko, Sugiura Yuki, Sato Kohji, Kugo Hirona, Moriyama Tatsuya, Konno Hiroyuki, Setou Mitsutoshi, Unno Naoki
Division of Vascular Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan; Department of Cell Biology and Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Japan; Second Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Department of Cell Biology and Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Japan; Department of Applied Biological Chemistry, Graduate School of Agriculture, Kinki University, Nara, Japan.
PLoS One. 2015 Aug 26;10(8):e0134386. doi: 10.1371/journal.pone.0134386. eCollection 2015.
The aortic wall is perfused by the adventitial vasa vasorum (VV). Tissue hypoxia has previously been observed as a manifestation of enlarged abdominal aortic aneurysms (AAAs). We sought to determine whether hypoperfusion of the adventitial VV could develop AAAs. We created a novel animal model of adventitial VV hypoperfusion with a combination of a polyurethane catheter insertion and a suture ligation of the infrarenal abdominal aorta in rats. VV hypoperfusion caused tissue hypoxia and developed infrarenal AAA, which had similar morphological and pathological characteristics to human AAA. In human AAA tissue, the adventitial VV were stenotic in both small AAAs (30-49 mm in diameter) and in large AAAs (> 50 mm in diameter), with the sac tissue in these AAAs being ischemic and hypoxic. These results indicate that hypoperfusion of adventitial VV has critical effects on the development of infrarenal AAA.
主动脉壁由外膜滋养血管(VV)供血。组织缺氧先前已被观察到是腹主动脉瘤(AAA)增大的一种表现。我们试图确定外膜VV灌注不足是否会导致AAA的发生。我们通过在大鼠中插入聚氨酯导管并结扎肾下腹主动脉,创建了一种新型的外膜VV灌注不足动物模型。VV灌注不足导致组织缺氧并形成肾下AAA,其具有与人类AAA相似的形态和病理特征。在人类AAA组织中,小AAA(直径30 - 49毫米)和大AAA(直径> 50毫米)的外膜VV均狭窄,这些AAA中的瘤壁组织缺血且缺氧。这些结果表明,外膜VV灌注不足对肾下AAA的发生具有关键影响。