AI Article Synopsis
- Delayed cerebral vasospasm is a critical issue following subarachnoid hemorrhage (SAH), linked to low nitric oxide levels and dysfunction of endothelial nitric oxide synthase (eNOS).
- Memantine, an NMDA blocker, has shown promise in reducing early brain injury from SAH and was tested for its effects on vasospasm and eNOS functionality.
- Results indicated that memantine successfully reduced vasospasm and improved eNOS function, suggesting potential for future treatment strategies in SAH-related vasospasm.
Article 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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4490546 | PMC |
| http://dx.doi.org/10.3390/ijms160614171 | DOI Listing |
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