http://content.karger.com/produktedb/pr ... doi=320624
Journal of Vascular Research
Vol. 48, No. 3, 2011
Venous Hypoxia: A Poorly Studied Etiological Factor of Varicose Veins
Venous hypoxia has long been postulated as a potential cause of varicosity formation. This article aimed to review the development of this hypothesis, including evidence supporting and controversies surrounding it. Vein wall oxygenation is achieved by oxygen diffusing from luminal blood and vasa vasorum. The whole media of varicosities is oxygenated by vasa vasorum as compared to only the outer two-thirds of media of normal veins. There was no evidence that differences exist between oxygen content of blood from varicose and non-varicose veins, although the former demonstrated larger fluctuations with postural changes. Studies using cell culture and ex vivo explants demonstrated that hypoxia activated leucocytes and endothelium which released mediators regulating vein wall remodelling similar to those observed in varicosities. Venoactive drugs may improve venous oxygenation, and inhibit hypoxia activation of leucocytes and endothelium. The evidence for hypoxia as a causative factor in varicosities remains inconclusive, mainly due to heterogeneity and poor design of published in vivostudies. However, molecular studies have shown that hypoxia was able to cause inflammatory changes and vein wall remodelling similar to those observed in varicosities. Further studies are needed to improve our understanding of the role of hypoxia and help identify potential therapeutic targets.
Copyright © 2010 S. Karger AG, Basel
Slowed perfusion is a known symptom found in brain MRI's of people with MS. If blood is leaving the brain in a more deoxiginated state because it is traveling through the brain more slowly due to CCSVI, and if that is causing venous hypoxia of the IJVs, azygous, and for that matter of the blood vessels in the brain itself, then this study seems to indicate that it could be causing the vein wall remodeling seen in MS (change from collegen 1 to collegen 3) and even triggering the MS inflamatory and autoimmune process (leucocytes).
I know varicose veins are not the same as stenosed jugular veins, but this recent study seems to point toward a similar process at work (at least that's how it seems to my cog fog impaired, though previously very bright brain). I think I remember reading that the shift from collegen 1 to collegen 3 seen in vein tissue samples of people with CCSVI, also occurs in people with varicose veins.
This study does bring an interesting question to mind: If we are born with venous "birth defects" (inverted valves, etc), would it be more effective to balloon them early in life, before the vein walls become less elastic due to vein wall remodeling because of venous hypoxia? Would early intervention be less likely to restenose than it would later in life once the vein wall has become stiffer?
Speculating wildly of course (I have not yet read that vein hypoxia is a part of CCSVI, and I am not a medical professional), but its interesting!