Isoflurane attenuates blood-brain barrier disruption in ipsilateral hemisphere after subarachnoid hemorrhage in mice.
Isoflurane attenuates blood-brain barrier disruption in ipsilateral hemisphere after subarachnoid hemorrhage in mice.
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DOI:
10.1161/strokeaha.112.661728
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发表时间:
2012-09
期刊:
影响因子:
8.3
通讯作者:
Zhang JH
中科院分区:
文献类型:
--
作者:
Altay O;Suzuki H;Hasegawa Y;Caner B;Krafft PR;Fujii M;Tang J;Zhang JH
We examined effects of isoflurane, volatile anesthetics, on blood-brain barrier (BBB) disruption in the endovascular perforation model of subarachnoid hemorrhage (SAH) in mice. Animals were assigned to sham-operated, SAH+vehicle-air, SAH+1% or 2% isoflurane groups. Neurobehavioral function, brain water content, Evans blue dye extravasation and Western blotting for sphingosine kinases (SphKs), occludin, claudin-5, junctional adhesion molecule and vascular endothelial cadherin were evaluated at 24 hours post-SAH. Effects of SphK (DMS) or sphingosine-1-phosphate receptor-1/3 (S1P1/3) inhibitors (VPC23019) on isoflurane's action were also examined. SAH aggravated neurological scores, brain edema and BBB permeability, which were prevented by 2% but not 1% isoflurane posttreatment. 2% isoflurane increased SphK1 expression and prevented a post-SAH decrease in expressions of the BBB-related proteins. Both DMS and VPC23019 abolished the beneficial effects of isoflurane. 2% isoflurane can suppress post-SAH BBB disruption, which may be mediated by SphK1 expression and S1P1/3 activation.