Memantine Attenuates Delayed Vasospasm after Experimental Subarachnoid Hemorrhage via Modulating Endothelial Nitric Oxide Synthase

被引:16
作者
Huang, Chih-Yuan [1 ,2 ]
Wang, Liang-Chao [1 ,2 ]
Shan, Yan-Shen [1 ,2 ]
Pan, Chia-Hsin [1 ]
Tsai, Kuen-Jer [1 ,3 ]
机构
[1] Natl Cheng Kung Univ, Coll Med, Inst Clin Med, Tainan 704, Taiwan
[2] Natl Cheng Kung Univ, Coll Med, Natl Cheng Kung Univ Hosp, Dept Surg, Tainan 704, Taiwan
[3] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Coll Med, Ctr Clin Med, Tainan 704, Taiwan
关键词
BARRIER PERMEABILITY CHANGES; CEREBRAL VASOSPASM; MELANOCORTINS; ACTIVATION; NO;
D O I
10.3390/ijms160614171
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:14171 / 14180
页数:10
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