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

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.