I believe in the animal model, intimal hyperplasia can reduced with high levels of oxygen. Do not think its been shown in humans.
Medial smooth muscle cells are considered target cells for vascular brachytherapy, and it has
been suggested that most of these targets cells are hypoxic. Several studies indicated that
medial cells of coronary arteries exist at least in part in a state of not only acute but also
chronic hypoxia. Physiologic studies in the late 1970s demonstrated that the entire avascular
media of a human thoracic aorta is chronically hypoxic, and that smoking can further reduce
oxygen tension in the media (Schneiderman et al. 1978). If a stent is deployed to the arterial
wall, hypoxia of medial smooth muscle cells increases, and returns to normal after a period
of 28 days in the rabbit (Santilli et al. 2000). Hypoxia stimulates proliferation of human
vascular smooth muscle cells (VSMCs) (Cooper et al. 1999), while supplemental oxygen
may reduce exaggerated proliferative responses in the vasculature (Lee et al. 2001).http://www.freidok.uni-freiburg.de/voll ... /diss1.pdf
Arteries not veins but intriguing.
Volume 185, Issue 2, Pages 254-263 (April 2006)http://tinyurl.com/4bsl55m
Intimal thickening after arterial balloon injury is increased by intermittent repetitive hypoxia, but intermittent repetitive hyperoxia is not protective
Antony K. Laua, Xavier Chaufourb, Craig McLachlanb, Steven B. Leichtweisa, David S. Celermajerac, Colin Sullivanb, Roland Stockerade
Hypoxia makes intimal hyperplasia worse, but hyperoxia does not make it better. If you are a bunny. In a single study.
Arterial intimal hyperplasia after occlusion of the adventitial vasa vasorum in the pig
SG Barker, A Talbert, S Cottam, PA Baskerville and JF Martin
Kings College School of Medicine and Dentistry, Department of Medicine, Denmark Hill, London, UK.
Oxygenation of the arterial wall is provided by diffusion of oxygen outward from the main vessel lumen and inward from the adventitial vasa vasorum. In a group of four Yucatan miniature pigs the oxygenation profiles across the superficial femoral arteries were recorded by polarographic oxygen microelectrodes. The profiles obtained suggested a relatively poorly oxygenated media (a trough value of approximately 25% that of the intimal oxygenation) with a progressive rise in oxygenation toward the intimal and adventitial surfaces. In four other survival experiments, occlusion of the adventitial vasa vasorum by flush ligation of the arterial branches that supply them resulted in the production of a focal, intimal hyperplastic lesion that was absent in control vessels (intimal to medial ratios [mean +/- SEM] of 0.053 +/- 0.008, n = 8, p < 0.001 and 0.013 +/- 0.001, n = 8, respectively). By electron microscopy this lesion was seen to be composed mainly of smooth muscle cells. This evidence would support the hypothesis that arterial wall hypoxia may be involved in the initiation of intimal hyperplasia. It is proposed that human atherosclerosis may be initiated by occlusion of the vasa vasorum and concomitant hypoxia.
Interesting lead (and at first I was doubtful).