Memantine Attenuates Delayed Vasospasm after Experimental Subarachnoid Hemorrhage via Modulating Endothelial Nitric Oxide Synthase
نویسندگان
چکیده
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.
منابع مشابه
Simvastatin Attenuates Experimental Cerebral Vasospasm and Ameliorates Serum Markers of Neuronal and Endothelial Injury in Patients After Subarachnoid Hemorrhage: A Dose-Response Effect Dependent on Endothelial Nitric Oxide Synthase
Delayed cerebral ischemic injury secondary to vasospasm is a major cause of morbidity and mortality after subarachnoid hemorrhage (SAH) (28). Currently, there are no medical treatments that consistently prevent or reverse cerebral vasospasm. Recent studies suggest vasospasm is the result of a multifactorial process leading to a functional imbalance in the cerebrovascular smooth muscle tone (9, ...
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