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Memantine Attenuates Delayed Vasospasm after Experimental Subarachnoid Hemorrhage
via Modulating Endothelial Nitric Oxide Synthase
#MMPMID26110388
Huang CY
; Wang LC
; Shan YS
; Pan CH
; Tsai KJ
Int J Mol Sci
2015[Jun]; 16
(6
): 14171-80
PMID26110388
show ga
Delayed cerebral vasospasm is an important pathological feature of subarachnoid
hemorrhage (SAH). The cause of vasospasm is multifactorial. Impairs nitric oxide
availability and endothelial nitric oxide synthase (eNOS) dysfunction has been
reported to underlie vasospasm. Memantine, a low-affinity uncompetitive
N-methyl-d-aspartate (NMDA) blocker has been proven to reduce early brain injury
after SAH. This study investigated the effect of memantine on attenuation of
vasospasm and restoring eNOS functionality. Male Sprague-Dawley rats weighing
350-450 g were randomly divided into three weight-matched groups, sham surgery,
SAH + vehicle, and SAH + memantine groups. The effects of memantine on SAH were
evaluated by assessing the severity of vasospasm and the expression of eNOS.
Memantine effectively ameliorated cerebral vasospasm by restoring eNOS
functionality. Memantine can prevent vasospasm in experimental SAH. Treatment
strategies may help combat SAH-induced vasospasm in the future.
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