View larger version (48K):
[in this window]
[in a new window]
|
FIGURE 6. Distinction of ML-10 uptake in infarct region from blood activity (A) and BBB disruption (B). (A) Kinetic profile of clearance of tracer from damaged hemisphere (DH) vs. blood (30–90 min after administration; activity at 30 min was defined as 100%). (B) Fluorescence microscopy showing transitional zone between healthy brain tissue (area A) and infarct (areas B and C). Animal was subjected to MCA occlusion; 24 h later, concomitant administration of fluorescent probe dansyl-ML-10 and EB (marker of BBB disruption) was performed. Area A contained intact brain tissue; therefore, it lacked EB or dansyl-ML-10 binding and manifested pale bluish autofluorescence. Area B contained cells at portion of infarct with BBB disruption, as indicated by EB extravasation to extracellular space, giving rise to red haze. Area C contained EB-negative cells, manifesting green fluorescence of dansyl-ML-10 and therefore indicating tracer uptake without concomitant BBB disruption. Uptake was cellular, into individual cells, creating starry-sky appearance of slide; this pattern is characteristic of apoptosis (magnification, x200).
|
-radiation–sensitive phosphorimaging plate revealed accumulation of 18F-ML-10 signal in brain area corresponding to ischemic MCA territory. Graded intensities were observed, with highest uptake at infarct core and gradually less uptake at periphery. (B and C) TUNEL staining of transitional zone between ischemic and healthy brain tissues (enlargements of inset in A; magnifications, x100 [B] and x200 [C]). 18F-ML-10 uptake was found to correlate with apoptosis, as indicated by TUNEL staining in corresponding region.