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, September 2, 2014

NOMI - Nitric oxide inhalation in heart attack patients sends mixed messages, but may offer benefit.

Nitric Oxide seems useful for stroke according to these research points. Whom is going to make a definitive statement about how and when NO is used in stroke? Anyone at all? Or are we just going to wait for somebody else to solve this problem?

Modulation of Adult Neurogenesis by the Nitric Oxide System

Efficacy of Nitric Oxide in Stroke' (ENOS) study 

Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury 

 

  Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury

 

  Regulation of Injury-Induced Neurogenesis by Nitric Oxide

 

 Nitric Oxide and the Biological Cascades Underlying Increased Neurogenesis, Enhanced Learning Ability, and Academic Ability as an Effect of Increased Bouts of Physical Activity

  Inhalation of nitric oxide could help improve blood flow to ischemic brain

  Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

 

  Cerebrovascular protection by various nitric oxide donors in rats after experimental stroke

 

Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function


 And here is the heart benefit.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=144932&CultureCode=en
Inhaled nitric oxide, delivered to heart attack patients before and during treatment with percutaneous coronary intervention (PCI) did not reduce the extent of damaged tissue (infarct), but may have improved recovery, according to Hot Line results presented today at ESC Congress 2014.
The NOMI (Nitric Oxide for inhalation to reduce reperfusion injury in acute st-elevation Myocardial Infarction) trial was based on the hypothesis that nitric oxide inhalation can reduce the injury caused to heart tissue during reperfusion (restoration of blood flow when a blocked artery is re-opened), according to Stefan Janssens, MD, PhD from University Hospital Gasthuisberg of Leuven, Belgium.
The trial included 250 heart attack patients with ST elevation myocardial infarction (STEMI) who presented between two and 12 hours after symptom onset.
Patients were randomised to receive supplemental oxygen via face mask, with (n=125) or without (n=125) nitric oxide at a concentration of 80 parts per million.
The gas was started in the catheterization laboratory prior to PCI and continued up to 4 hours after the start of reperfusion.
Magnetic resonance imaging (MRI) was used to measure infarct size, assessed as a fraction of left ventricular (LV) mass, as well as to evaluate LV remodeling (injury-related changes).
The study found that between 48-72 hours after the procedure there were no differences in infarct size between patients who received nitric oxide and those who did not (18% vs 19.4%, P=0.44).
However, a pre-specified sub-group analysis of patients who had received intracoronary or intravenous nitroglycerin (IC/IV NTG) – the administration of which was left to the discretion of the local investigators- showed a significant interaction  (P=0.014) with the use of inhaled nitric oxide. Among NTG-naïve patients (n=132), nitric oxide inhalation was associated with significantly smaller infarcts compared to patients who had previously received NTG (n=93).
In the total population, MRI at 48-72 hours showed a trend for improved LV functional recovery with nitric oxide, which became significant at 4 months (P=0.048).
Functional recovery was significantly better with nitric oxide in the sub-group of NTG-naïve patients.
Nitric oxide did not cause major adverse events, and for a secondary composite endpoint of death, recurrent ischemia, stroke or rehospitalisations it was associated with a trend towards a lower event rate (P=0.10).
The NOMI trial is the first to investigate the impact of nitric oxide inhalation on myocardial reperfusion injury, infarct size, and cardiac recovery, said Professor Janssens.
“While it did not show a significant reduction in infarct size in the overall study population, the findings suggest that nitric oxide inhalation merits further investigation in STEMI patients,” he concluded.

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