Neurovascular Protection Reduces Early Brain Injury After Subarachnoid Hemorrhage

S. Park
2004 Stroke  
and Purpose-Cell death, especially apoptosis, occurred in brain tissues after subarachnoid hemorrhage (SAH). We examined the relationships between apoptosis and the disruption of blood-brain barrier (BBB), brain edema, and mortality in an established endovascular perforation model in male Sprague-Dawley rats. Methods-A pan-caspase inhibitor (z-VAD-FMK) was administered intraperitoneally at 1 hour before and 6 hours after SAH. Expression of caspase-3 and positive TUNEL was examined as markers
more » ... mined as markers for apoptosis. Results-Apoptosis occurred mostly in cerebral endothelial cells, partially in neurons in the hippocampus, and to a lesser degree in the cerebral cortex. Accordingly, increased BBB permeability and brain water content were observed, accompanied by neurological deficit and a high mortality at 24 hours after SAH. z-VAD-FMK suppressed TUNEL and caspase-3 staining in endothelial cells, decreased caspase-3 activation, reduced BBB permeability, relieved vasospasm, abolished brain edema, and improved neurological outcome. Conclusions-The major effect of z-VAD-FMK on early brain injury after SAH was probably neurovascular protection of cerebral endothelial cells, which results in less damage on BBB. (Stroke. 2004;35:2412-2417.) Key Words: apoptosis Ⅲ blood-brain barrier Ⅲ brain edema Ⅲ subarachnoid hemorrhage
doi:10.1161/01.str.0000141162.29864.e9 pmid:15322302 fatcat:xkd655cnfvgldlo2xiy3i7iyim