Deans' stroke musings: Angiogenesis at short and longer intervals post ischemia: Relationship to neuroprotective actions of resveratrol

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.

Wednesday, January 25, 2012

Angiogenesis at short and longer intervals post ischemia: Relationship to neuroprotective actions of resveratrol

So does this mean wine would be good for you to protect against the cascade of death?
Ask your doctor. I can just see the ER nurses feeding you wine while still in the ICU.
Ok, not viable, in the order of one milligram per glass. From the 2011 Canadian Stroke Congress.
page 127 here:
http://www.strokecongress.org/2011/wp-content/uploads/2011/12/CSC_Abstracts.pdf
Background: Angiogenesis, or the formation of new blood vessels, is an essential element of brain developmentand health. Resveratrol (RSV) is a naturally occurring polyphenol phytoalexin that has an array of beneficial health effects and that has been shown to protect the brain against ischemic injury. However, whether
protection at the neuronal level is associated with plastic changes in brain organization post stroke or with recovery from cognitive impairments remains unknown. The present study examined the effects of 21-day RSV pre-treatment (1 or 10 mg/kg dose; i.p.) on ischemia-induced CA1 neuronal cell loss, angiogenesis levels in the hippocampus and behavioural impairment following 10 min global ischemia at 7 and 85 days post ischemia.
Methods: Male Wistar rats were divided into five groups, namely, sham + saline, ischemia + saline, ischemia + 1 mg/kg RSV, ischemia + 10 mg/kg RSVand sham + 10 mg/kg RSV. 7 or 85 days post surgery, brains were perfused and histopathological damage in the hippocampus determined. Immunohistochemical assessment of angiogenesiswas performed using Endothelial cell adhesion molecule-1 (CD-31)-labelling of blood vessels. Spatial working and reference memory were assessed using delayed non-matching or matching radial arm maze tasks.
Results: Our findings indicated significant neuroprotection by RSV at both time points investigated. Behaviorally, administration of 10 mg/kg RSV failed to improve ischemia-induced spatial memory deficits on either of the maze tasks, suggesting dose-dependent effect of RSV. We also show an increase in CD-31 expression in RSVtreated compared to saline-treated ischemic rats 7 and 85 days post injury. Noteworthy, angiogenesis was not restricted to areas most affected by ischemic injury (i.e., CA1 layer), suggesting complex relationships between angiogenesis and stroke recovery. Conclusion: This study demonstrates that RSV has the ability to protect CA1
neurons against ischemic injury, a phenomenon possibly promoted by increased angiogenesis.