Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,164 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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, October 30, 2018
Ischemic Stroke Increases Heart Vulnerability to Ischemia-Reperfusion and Alters Myocardial Cardioprotective Pathways
What EXACTLY is your stroke doctor and hospital doing to ensure this problem is solved? Sitting on their asses sucking their thumbs, most likely? They need to solve this since it is most likely contributing to 30 day stroke deaths.
For
years, the relationship between cardiac and neurological ischemic
events has been limited to overlapping pathophysiological mechanisms and
common risk factors. However, acute stroke may induce dramatic changes
in cardiovascular function. The aim of this study was to evaluate how
prior cerebrovascular lesions affect myocardial function and signaling
in vivo and ex vivo and how they influence cardiac vulnerability to
ischemia-reperfusion injury.
Methods—
Cerebral
embolization was performed in adult Wistar male rats through the
injection of microspheres into the left or right internal carotid
artery. Stroke lesions were evaluated by microsphere counting, tissue
staining, and assessment of neurological deficit 2 hours, 24 hours, and 7
days after surgery. Cardiac function was evaluated in vivo by
echocardiography and ex vivo in isolated perfused hearts. Heart
vulnerability to ischemia-reperfusion injury was investigated ex vivo at
different times post-embolization and with varying degrees of
myocardial ischemia. Left ventricles (LVs) were analyzed with Western
blotting and quantitatve real-time polymerase chain reaction.
Results—
Our
stroke model produced large cerebral infarcts with severe neurological
deficit. Cardiac contractile dysfunction was observed with an early but
persistent reduction of LV fractional shortening in vivo and of LV
developed pressure ex vivo. Moreover, after 20 or 30 minutes of global
cardiac ischemia, recovery of contractile function was poorer with
impaired LV developed pressure and relaxation during reperfusion in both
stroke groups. Following stroke, circulating levels of catecholamines
and GDF15 (growth differentiation factor 15) increased. Cerebral
embolization altered nitro-oxidative stress signaling and impaired the
myocardial expression of ADRB1 (adrenoceptor β1) and cardioprotective
Survivor Activating Factor Enhancement signaling pathways.
Conclusions—
Our
findings indicate that stroke not only impairs cardiac contractility
but also worsens myocardial vulnerability to ischemia. The underlying
molecular mechanisms of stroke-induced myocardial alterations after
cerebral embolization remain to be established, insofar as they may
involve the sympathetic nervous system and nitro-oxidative stress.
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