Hypoxia at the site of abdominal aortic aneurysm rupture is not associated with increased lactate

被引:21
作者
Choke, Edward [1 ]
Cockerill, Gillian W. [1 ]
Dawson, Joseph [1 ]
Chung, Yuen-Li [1 ]
Griffiths, John [1 ]
Wilson, Richard W. [1 ]
Loftus, Ian M. [1 ]
Thompson, Matthew M. [1 ]
机构
[1] Univ London St Georges Hosp, Acad Vasc Surg Unit, Dept Cardiovasc Sci, London SW17 0QT, England
来源
ABDOMINAL AORTIC ANEURYSM: GENETICS, PATHOPHYSIOLOGY AND MOLECULAR BIOLOGY | 2006年 / 1085卷
关键词
hypoxia; glycolysis; lactate; protein synthesis; abdominal aortic aneurysm; rupture;
D O I
10.1196/annals.1383.005
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 [理学]; 0710 [生物学]; 09 [农学];
摘要
The mechanisms of hypoxia-mediated aneurysm wall weakening and rupture are unknown. During hypoxia, strategies to maintain cellular ATP levels include increasing glycolysis (glycolytic strategy) or decreasing ATP consumption (metabolic depression). This study demonstrated that compared to anterior aneurysm sac, rupture edge overexpressed hypoxia-inducible factor-1-alpha (marker of hypoxia) and showed no significant difference in levels of combined ADP and ATP or lactate (glycolytic end product). Further studies are needed to confirm whether hypoxic AAA cells adapt through metabolic depression rather than glycolysis. The downregulation of protein synthesis during such metabolic depression may be a factor in hypoxia-mediated wall weakening.
引用
收藏
页码:306 / 310
页数:5
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