期刊
NEUROSCIENCE
卷 167, 期 1, 页码 60-67出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2010.01.053
关键词
aquaporin-4; astrocyte; brain edema; mouse model; subarachnoid hemorrhage; water channel
资金
- Royal College of Surgeons of England
- London Deanery
- Harrison Fund
- Neurosciences Research Foundation
- National Institutes of Health
- Guthy-Jackson Foundation
We investigated the role of the glial water channel protein aquaporin-4 in brain edema in a mouse model of subarachnoid hemorrhage in which 30 ill of blood was injected into the basal cisterns. Brain water content, intracranial pressure and neurological score were compared in wildtype and aquaporin-4 null mice. We also measured blood-brain barrier permeability, and the osmotic permeability of the glia limitans, one of the routes of edema elimination. Wildtype and aquaporin-4 null mice had comparable baseline brain water content, intracranial pressure and neurological score. At 6 h after blood injection, aquaporin-4 null mice developed more brain swelling than wildtype mice. Brain water content increased by 1.5 +/- 0.1% vs. 0.5 +/- 0.2% (Mean +/- Standard Error, P<0.0005) and intracranial pressure by 36 5 vs. 21 3 mm Hg (P<0.05) above pre-injection baseline, and neurological score was worse at 18.0 vs. 24.5 (median, P<0.05), respectively. Although subarachnoid hemorrhage produced comparable increases in blood brain barrier permeability in wildtype and aquaporin-4 null mice, aquaporin-4 null mice had a twofold reduction in glia limitans osmotic permeability. We conclude that aquaporin-4 null mice manifest increased brain edema following subarachnoid hemorrhage as a consequence of reduced elimination of excess brain water. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
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