Journal
STROKE
Volume 35, Issue 10, Pages 2412-2417Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.STR.0000141162.29864.e9
Keywords
apoptosis; blood-brain barrier; brain edema; subarachnoid hemorrhage
Categories
Funding
- NINDS NIH HHS [NS45694] Funding Source: Medline
Ask authors/readers for more resources
Background 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 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available