Acute Physiologic and Morphologic Assessment Following Subarachnoid Hemorrhage - Animal Models of Acute Neurological Injuries: Injury and Mechanistic Assessments - page 295

Fig. 4. Photomicrographs of Fluoro-Jade B stained sections and confocal microscopy
following MCAO. Damaged neurons within the infracted region are fl uorescently stained
( green ) while surviving neurons within the pneumbra are left unstained (scalebar = 100 m).
Frames 3-6, confocal microscopy of vascular permeability markers dextran (70 kDa) and
fi brinogen (300 kDa) 24 h post-MCAO and rt-PA reperfusion, taken in the penumbral region
of the infarct. Frames 3 and 4, confocal images of fi brinogen ( red ) and dextran ( green )
reactivity in the ipsilateral cortex. No dextran extravasation is observed in frame 3 and is
similar to images from contralateral hemisphere in frame 5. Dextran is present in the
extracellular space frame 4 animals at the same time point. Frame 6, image in bright fi eld
that depicts lumen of cerebral microvessel. Fibrinogen can be seen remaining within the
lumen of the vessel while dextran reactivity is present along the outer surface in animal
that underwent MCAO and rt-PA reperfusion (scale bar = 5 μ m). (DiNapoli et al. 2008).
3. Early Changes
Aneurysmal rupture confers immediate effects on the surrounding
tissue; recent theories have begun to describe these acute events as
early brain injury (EBI). EBI results from decreased CBF and
perfusion pressure mediated by increased ICP and acute vasocon-
striction ( 5 ). Destruction of the microvascular architecture aug-
ments global ischemia and initiates a cascade of cellular injury.