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Abstract
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.
Highlights
Subarachnoid hemorrhage (SAH) accounts for 5%–10% of all cerebrovascular accidents and is a major cause of disability and death in humans [1]
The present study examined the therapeutic effects of memantine in SAH-induced endothelial dysfunction and delayed vasospasm
To examine the effect of memantine on attenuation of delayed vasospasm after SAH, the lumen area of the basilar artery was measured for each group as shown in the corresponding bar graphs (Figure 2)
Summary
Subarachnoid hemorrhage (SAH) accounts for 5%–10% of all cerebrovascular accidents and is a major cause of disability and death in humans [1]. Nitric oxide (NO), a diffusible factors and a powerful dilator, causes a number of beneficial effects such as antithrombotic effects, prevention of excess platelet adhesion and aggregation, maintenance of vascular tone and regulation of cerebral blood flow [3,4] It activates soluble guanylyl cyclase and up-regulates 3ʹ–5ʹ cGMP and dilates the arteries in response to metabolic demand and shear stress. A low-affinity uncompetitive NMDA blocker, has been shown to be effective in preventing neuronal damage after models of neurological injury [10], including SAH [11] It has been reported memantine attenuated production of reactive oxygen species after SAH by diminishing the impairment of neurovascular units and preserving the integrity brain-blood barrier [11]. The present study examined the therapeutic effects of memantine in SAH-induced endothelial dysfunction and delayed vasospasm
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