Fig. 2.
The bimodal role of AQP4 in the pathomechanism of cerebral edema. (a) Electron micrographs demonstrating pronounced perivascular astrocyte foot process swelling (arrows) 30 min after acute water intoxication in wild-type mice, whereas AQP4−/− mice lack cytotoxic cell swelling. (bar=3µm) (b) Wild-type mice show accelerated brain swelling and intracranial pressure increase (ICP) compared to AQP4−/− mice following IP water intoxication. Increased brain water uptake in wild-type mice is demonstrated by higher relative ICP elevation at 10 min (ΔICP10 min) and significantly shorter time required to reach maximal ICP value (time to [dICP/dt]max). (c) Reduced hemispheric enlargement in AQP4−/− mice compared to wild type controls 24 h following permanent MCA occlusion. Note the midline shift in the wild- type brain (arrow). (d) Improved functional outcome 24 h after MCA occlusion in AQP4−/−mice. (e) Cortical freeze injury disrupts the blood–brain barrier as assessed by Evans Blue extravasation and causes vasogenic edema. (f) Brain water content increase in AQP4−/− mice compared to wild-type controls in vasogenic edema