Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Tuesday, February 14, 2017

Intermittent hypobaric hypoxia preconditioning protects against acute severe hypoxic damage in brain

So prior to your stroke you would need to be pretreated with this. So start planning your stroke now. Or you could just live at a higher elevation. But the reduction in nitric oxide levels does not seem like a good thing.

High altitudes for Training the Brain to Survive Stroke.

Intermittent hypobaric hypoxia preconditioning protects against acute severe hypoxic damage in brain

D. Coimbra-Costa1, N. Alva1, T. Carbonell1, R. Rama1
1. Biologia cel.lular, Fisiologia i Immunologia, Universitat de Barcelona, Barcelona, Catalonia, Spain.

Acute severe hypoxia (SH) causes an increase in oxidative stress and apoptosis in the brain. In contrast, intermittent hypobaric hypoxia (IHH) can increase brain antioxidant capacity and result in neuroprotection, as we previously reported (Costa et al., 2013). Thus, the present work uses IHH as preconditioning against damage potentially induced by SH. Adult rats were divided into four groups: 1) controls; 2) SH group, subjected to 6 h of acute hypoxia at 7% oxygen; 3) IHH group, exposed to 380 mmHg (equivalent to an altitude of 4000 m) in a hypobaric chamber, 4 h/day for 8 days; and 4) combined IHH-SH group, subjected to acute SH (7% oxygen) for 6 h after the last IHH exposure. Animals were anesthetized with isoflurane inhalation and then sacrificed.The brains were extracted and compared to controls.The study was approved and authorized by the Institutional Committee of Animal Care and Research of the University of Barcelona. The experimental protocol follows the European Community guidelines. SH induced oxidative stress in the brain, as indicated by increased levels of oxidized proteins, lipid peroxidation, inducible nitric oxide synthase (iNOS) expression and nitric oxide metabolites. This acute hypoxic also resulted in glutathione depletion and increased glutathione peroxidase. As for the apoptosis parameters studied, SH increased cytochrome c in the brain, and the activity of caspase 3 in the brain cortex and hippocampus. The IHH preconditioning protocol induced the expression of HIF-1 without causing oxidative stress or apoptosis, and induced expression of neuroprotective proteins such as EPO and VEGF. The IHH reduced nitric oxide levels by 28%, the content of oxidized proteins by 30% and lipid peroxidation values by 48%. It also better preserved the ratio of oxidized/reduced glutathione in brain tissue. Our study thereby demonstrates that IHH is a useful way to prepare the brain to tolerate the effects of SH better, maintaining antioxidant activity and mitochondrial function, and promoting the expression of neuroprotective factors.

Where applicable, experiments conform with Society ethical requirements

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