Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 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:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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 lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, March 5, 2013

Is cerebral oxygenation negatively affected by infusion of norepinephrine in healthy subjects?

If all the HBOT pushers are correct in that extra oxygenation will help save neurons then this method would be lots easier and cheaper. Your doctor should know the answer, its only been published 4 years ago.  You do think your doctor is less than 4 years out-of-date? Don't you?
http://bja.oxfordjournals.org/content/102/6/800

Abstract

Background Vasopressor agents are commonly used to increase mean arterial pressure (MAP) in order to secure a pressure gradient to perfuse vital organs. The influence of norepinephrine on cerebral oxygenation is not clear. The aim of this study was to evaluate the impact of the infusion of norepinephrine on cerebral oxygenation in healthy subjects.
Methods Three doses of norepinephrine (0.05, 0.1, and 0.15 µg kg−1 min−1 for 20 min each) were infused in nine healthy subjects [six males; 26 (6) yr, mean (sd)]. MAP, cerebral oxygenation characterized by frontal lobe oxygenation (Sco2) and internal jugular venous oxygen saturation (Sjvo2), middle cerebral artery mean flow velocity (MCA Vmean), cardiac output (CO), and arterial partial pressure for carbon dioxide (Paco2) were evaluated.
Results MAP increased from 88 (79–101) [median (range)] to 115 (98–128) mm Hg with increasing doses of norepinephrine (P < 0.05), reflecting an increase in total peripheral resistance [20.3 (12.2–25.8) to 25.2 (16.4–28.5) mm Hg min litre−1; P < 0.05] since CO remained at baseline values. Sco2 and Sjvo2 decreased with increasing doses of norepinephrine, reaching statistical significance with norepinephrine infused at 0.1 µg kg−1 min−1 [Sco2: 78 (75–94) to 69 (61–83)%; P < 0.05; Sjvo2: 67 (8) to 64 (7)%; P < 0.01]. MCA Vmean was reduced with each dose of norepinephrine [56.9 (11.2) to 55.0 (11.7) cm s−1; P < 0.05] and Paco2 lowered from 5.4 (0.4) to 5.1 (0.4) kPa (P < 0.001).
Conclusions This study suggests that infusion of norepinephrine at 0.1 µg kg−1 min−1 or higher may negatively affect cerebral oxygenation.

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