Hypoperfusion of the Adventitial Vasa Vasorum Develops an Abdominal Aortic Aneurysm

PLoS One. 2015 Aug 26;10(8):e0134386. doi: 10.1371/journal.pone.0134386. eCollection 2015.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Animals
  • Aorta, Abdominal / metabolism
  • Aorta, Abdominal / pathology
  • Aorta, Abdominal / physiopathology
  • Aortic Aneurysm, Abdominal / complications
  • Aortic Aneurysm, Abdominal / metabolism
  • Aortic Aneurysm, Abdominal / pathology
  • Aortic Aneurysm, Abdominal / physiopathology*
  • Blood Circulation*
  • Constriction, Pathologic / complications
  • Female
  • Humans
  • Male
  • Oxygen / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Vasa Vasorum / metabolism
  • Vasa Vasorum / pathology
  • Vasa Vasorum / physiopathology*

Substances

  • Oxygen

Grants and funding

This work was supported by Grants-in-Aid for Scientific Research (B) (20291958) to NU, (C) (26462103) to KI; Grants-in-Aid for Young Scientists (A) (25713024) to NZ; a Grant-in-Aid for SENTAN from the Japan Science and Technology Agency (JST); Tokutei Lipid Machinery; and Young Scientists S (2067004) to M. Setou. Financial support for overseas study was provided by the Japan Research Foundation for Clinical Pharmacology to HT.