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.
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