When we need to get drugs thru the blood-brain barrier we might be able to use this method.
http://www.dovepress.com/articles.php?article_id=9949
Purpose: We evaluated the
delivery efficiency of intravenously injected large molecular agents,
before and after disruption of the blood–brain barrier (BBB-D), induced
by focused ultrasound (FUS) using various acoustic parameters.
Materials and methods:
Male Sprague-Dawley rats were injected intravenously with Evans blue
(EB) before or after BBB-D induction by pulsed FUS. We used a 1.0 MHz
pulsed FUS with four acoustic power settings and an ultrasound contrast
agent (UCA) at four different doses to induce BBB-D resulting from
cavitation. The permeability of the BBB was assessed quantitatively
based on the extravasation of EB. Contrast enhanced magnetic resonance
imaging (MRI) was used to monitor the gadolinium deposition associated
with FUS. Histological analysis was performed to examine tissue damage.
Results:
The accumulation of EB in rat brain was found to be dependent on
acoustic power and UCA dosage, regardless of whether EB administration
occurred before or after FUS-induced BBB-D. Administration of EB
followed by sonication resulted in greater EB extravasation than that
for rats subjected to sonication prior to EB injection. To reduce tissue
damage, EB extravasation was enhanced by first administering EB by
intravenous injection, followed by sonication at reduced acoustic power
or UCA dosage. The normalized signal intensity change in rat brains that
received the same dose of UCA and sonicated after gadolinium injection
was significantly greater than in rats undergoing sonication followed by
gadolinium administration. Moreover, contrast enhanced MRI showed a
more precise distribution of gadolinium in the brain when gadolinium was
administered before sonication.
Conclusion: We
demonstrated that a compound administered prior to sonication treatment
promotes extravasation of the sonicated region. Thus, it is possible to
optimize ultrasound parameters for lower sonication and reduced UCA
doses, to induce BBB-D while minimizing damage to normal brain tissue.
Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 28,972 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 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.
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