Deans' stroke musings: Roles of Nitric Oxide in Brain Ischemia and Reperfusion

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.

Friday, April 15, 2022

Roles of Nitric Oxide in Brain Ischemia and Reperfusion

EXACTLY WHOM WILL BE DOING THE FOLLOWUP RESEARCH ON THIS? Since there is NO stroke leadership, nothing is ever done to solve stroke. You'll have to tell your children and grandchildren to never have a stroke since they are effectively untreatable, contrary to this lie from World Stroke Day a few years ago.

What a lying piece of shit.

Roles of Nitric Oxide in Brain Ischemia and Reperfusion

Yijie Wang 1,2 , Fenfang Hong 1,* and Shulong Yang 3,* 1 Experimental Center of Pathogen Biology, College of Medicine, Nanchang University, Nanchang 330047, China; yijiewyj0406@163.com 2 Queen Mary University of London Nanchang Joint Program, Medical College, Nanchang University, Nanchang 330006, China 3 Department of Physiology, Fuzhou Medical College, Nanchang University, Fuzhou 344099, China * Correspondence: hongfenfang@126.com (F.H.); yangshulong315@139.com or shulongyang@aliyun.com (S.Y.)

Abstract:

Brain ischemia and reperfusion (I/R) is one of the most severe clinical manifestations of ischemic stroke, placing a significant burden on both individuals and society. The only FDA-approved clinical treatment for ischemic stroke is tissue plasminogen activator (t-PA), which rapidly restores cerebral blood flow but can have severe side effects. The complex pathological process of brain I/R has been well-established in the past few years, including energy metabolism disorders, cellular acidosis, doubling of the synthesis or release of excitotoxic amino acids, intracellular calcium homeostasis, free radical production, and activation of apoptotic genes. Recently, accumulating evidence has shown that NO may be strongly related to brain I/R and involved in complex pathological processes. This review focuses on the role of endogenous NO in pathological processes in brain I/R, including neuronal cell death and blood brain barrier disruption, to explore how NO impacts specific signaling cascades and contributes to brain I/R injury. Moreover, NO can rapidly react with superoxide to produce peroxynitrite, which may also mediate brain I/R injury, which is discussed here. Finally, we reveal several therapeutic approaches strongly associated with NO and discuss their potential as a clinical treatment for ischemic stroke.