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, April 8, 2014

Enhanced endothelial nitric oxide production impairs cerebrovascular tone after brain trauma

You'll have to ask your doctor what the problem is and the solution proposed.  There has to be some reason this research was done.
http://www.fasebj.org/content/28/1_Supplement/1070.1.short
  1. Kalev Freeman1
+ Author Affiliations
  1. 1Phamacology University of Vermont Burlington VT United States

Abstract

Enhancend endothelial nitric oxide production impairs cerebrovascular tone after brain trauma Nuria Villalba, Thomas Longden, Mark T. Nelson, George C. Wellman and Kalev Freeman Department of Pharmacology, University of Vermont, Burlington, VT Cerebral autoregulation is altered after traumatic brain injury (TBI) reflecting an impairment in myogenic tone and that may contributeing to patient morbidity in patients with TBI. We hypothesized that TBI alters nitric oxide (NO)-dependent signaling mechanisms leading to decreased cerebral vascular tone. We studied isolated cerebral arteries from adult rats after moderate fluid percussion TBI or sham surgery. We found that both endothelial and smooth muscle (SM) NO levels—indexed by 4,5-diaminofluorescein (DAF-2) fluorescence—were increased in cerebral arteries from TBI animals. Arteries from TBI animals exhibited decreased cytosolic SM Ca2+ and reduced myogenic tone compared to controls. Endothelial removal restored myogenic response constriction in TBI animals. Further, inhibition of NO synthase with Nω-L-arginine (L-NNA) restored both myogenic tone and SM Ca2+, and reduced DAF-2 fluorescence in arteries from TBI animals. The guanylyl cyclase inhibitor (ODQ) and protein kinase G (PKG) inhibitor (RP-8-Br-cGMPS) both elicited robust enhanced constrictions in TBI animals. Further, constriction caused by inhibition of SM large-conductance Ca2+-activated potassium (BK) channels with paxilline was augmented in TBI arteries. Addition of 30 nM clamped NO to control arteries provided vasodilation equivalent to that observed in TBI and increased the DAF-2 signal to a comparable level observed in untreated TBI preparations. These data demonstrate that trauma causes persistent changes in endothelial NO production underlying profound cerebral artery dilation, and provides a quantitative measure of the degree of NO elevation, which is on the order of 30 nM. 

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