mjc701 wrote: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
Volume 185, Issue 2, Pages 254-263 (April 2006)
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
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.
The recent publicity given to the work of Professor Paolo Zamboni has highlighted a growing disaffection with the concept of ‘auto’ immunity which has dominated MS research and treatment for more than half a century.... However, the use of an animal model for MS research after WW2 led to the concept of auto immunity where, it is claimed, the immune system attacks normal tissue. Despite sixty years of research there is no evidence of this and it remains just a theory.
What is certain is the damage in MS involves veins and inflammation and Professor Zamboni has focused on these proven observations. He noticed, when using ultrasound scanning of the neck in a Multiple Sclerosis patient, that blood flowed the wrong way in a vein and also that the vein appeared to be constricted. After more investigations he has used the same procedure used to stretch arteries in the heart to relieve the vein constrictions. Several patients have found the procedure beneficial, greatly reducing their symptoms although stretching the veins will not affect existing scarring.
Professor Zamboni’s work has highlighted the importance of the blood-brain barrier. Oxygen is responsible for the genetic control of inflammation and lack of oxygen has been shown in affected areas in MS patients by brain imaging. Neurologists are likely to remain sceptical of vein stretching until a ‘controlled’ study is done in which a sham procedure is used and compared to a group of matched patients who have the real procedure undertaken.
Philip B James MB ChB DIH PhD FFOM
Emeritus Professor of Medicine University of Dundee
Honorary Medical Adviser MS Therapy Centre
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