Thursday, 19 September 2013

More Oxygen Please, it'll do wonders for my relapse

Davies AL, Desai RA, Bloomfield PS, McIntosh PR, Chapple KJ, Linington C, Fairless R, Diem R, Kasti M, Murphy MP, Smith KJ.
Neurological deficits caused by tissue hypoxia in neuroinflammatory disease. Ann Neurol. 2013 Aug. doi: 10.1002/ana.24006. [Epub ahead of print]

To explore the presence and consequences of tissue hypoxia in experimental autoimmune encephalomyelitis ((EAE), an animal model of multiple sclerosis (MS)).
METHODS: EAE was induced in Dark Agouti (DA) rats by immunization with recombinant myelin oligodendrocyte glycoprotein (rMOG) and adjuvant. Tissue hypoxia was assessed in vivo using two independent methods: an immunohistochemical probe administered intravenously, and insertion of a physical, oxygen-sensitive probe into the spinal cord. Indirect markers of tissue hypoxia (e.g. expression of hypoxia-inducible factor-1α (HIF-1α), vessel diameter and number) were also assessed. The effects of brief (one hour) and continued (7 days) normobaric oxygen treatment on function were evaluated in conjunction with other treatments, namely administration of a mitochondrially-targeted antioxidant (MitoQ) and inhibition of inducible nitric oxide synthase (1400W).
RESULTS: Observed neurological deficits were quantitatively, temporally and spatially correlated with spinal white and grey matter hypoxia. The tissue expression of HIF-1α also correlated with loss of function. Spinal microvessels became enlarged during the hypoxic period, and their number increased at relapse. Notably, oxygen administration significantly restored function within one hour, with improvement persisting at least one week with continuous oxygen treatment. MitoQ and 1400W also caused a small but significant improvement.
INTERPRETATION: We present chemical, physical, immunohistochemical and therapeutic evidence that functional deficits caused by neuroinflammation can arise from tissue hypoxia, consistent with an energy crisis in inflamed CNS tissue. The neurological deficit was closely correlated with spinal white and grey matter hypoxia. This realization may indicate new avenues for therapy of neuroinflammatory diseases such as MS.

This study suggests that there is lack of oxygen in tissues during EAE, which has nothing to do with CCSVI, and if you give rats high amounts of oxygen they do better 

10 comments:

  1. From your point of view, would it make sense to get into a hyperbaric chamber during a relapse? (given the fact it would not hurt you and according to this study it might help you)

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    1. I believe hyperbaric oxygen helps to speed up the recovery of an illness. I've been having the therapy for over two years now.

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    2. Hyperbaroc oxygen is oxygen at high pressure. In air there is about 20% oxygen this is talking about 100%. So make sure you dont strike a match

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  2. I hope Big Pharma pursues this. There are drugs that increase cerebral perfusion. If such a drug could improve neurological deficits associated with MS hypoxia in humans and not just rats, then this could be used adjunctively with the current MS drugs (and adjunctively with treatment of any vascular abnormalities). Relieving hypoxia caused by neuroinflammation could potentially result in reduced neuron death. This is exciting research, I would like to see it taken further.

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  3. An oxygen tank would not be a big incentive for pharma,it is about oxygenation and not really perfusion

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  4. MD, could you possibly explain further what you mean by 'oxygenation' in this case and in respect of humans? Is it because the human brain is a "oxygen guzzler", and uses most of it in synaptic transmission?

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  5. Yep the brain is an oxygen guzzler it is the fuel of the brain as it is vital for energy production, give the engine fuel and it can work.

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  6. Could it help alleviate a relapse....this needs a formal study.

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  7. Or could it prevent a relapse. That would be even better.

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  8. 'Hyperbaric Oxygen Therapy' (HBOT) or as they prefer to call it now 'High Density Oxygen Therapy' (HDOT) works simply by oxygenating the blood to a much higher density, than at lower pressures by dramatically high amounts. It is a bit like the OPPOSITE of what happens when you undo the top of a bottle of fizzy pop, and release and lower the pressure.
    The gas (CO2) comes out of suspension because of the reduction in pressure, sometimes quite dramatically. Once pressurised again, the gas will go back into the fluid.
    Increased pressure on the bodies blood to hold many times more Oxygen, than at lower pressures. makes it possible for the body to

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