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首页> 外文期刊>British journal of neurosurgery >Nebivolol attenuates cerebral vasospasm both by increasing endothelial nitric oxide and by decreasing oxidative stress in an experimental subarachnoid haemorrhage
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Nebivolol attenuates cerebral vasospasm both by increasing endothelial nitric oxide and by decreasing oxidative stress in an experimental subarachnoid haemorrhage

机译：Nebivolol通过增加内皮型一氧化氮并通过降低实验性蛛网膜下腔出血中的氧化应激来衰减脑血管痉挛

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Objective: Evidence suggests that reduction of nitric oxide (NO) bioavailability due to oxidative stress plays a central role in the pathophysiology of cerebral vasospasm after subarachnoid haemorrhage (SAH). To prevent SAH-induced cerebral vasospasm, therefore we used nebivolol hydrochloride as a NO-mediated vasodilator and an antioxidant drug in an experimental rat model of SAH.Materials and methods: Forty female Wistar rats were divided into control, SAH, SAH plus placebo, and SAH plus nebivolol groups. Starting six hours after inducing SAH, 5mg/kg of nebivolol hydrochloride and of pharmaceutical excipients of nebivolol was given orally once daily for five days to SAH plus nebivolol and SAH plus placebo groups, respectively. The lumen diameter and vessel wall thickness of the basilar artery were measured in brain sections. The serum and brain supernatant levels of nitric oxide (NO) were analysed. The brain supernatant levels of intrinsic antioxidants superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as markers of the antioxidant status.Results: Nebivolol administration attenuated cerebral vasospasm both by increasing NO levels and by decreasing oxidative stress. Our study also demonstrated that nebivolol administration reverses SAH created imbalance between SOD and GSH-Px by increasing GSH-Px activity relative to SOD.Conclusions: Nebivolol attenuates the cerebral vasospasm after SAH both increasing NO levels and decreasing oxidative stress. Therefore, it may promise to prevent SAH-induced cerebral vasospasm as an anti-spasmodic and anti-oxidant agent.
机译：目的：证据表明，由于氧化应激因氧化应激而降低一氧化物（NO）生物利用度在蛛网膜下腔（SAH）后脑血管痉挛的病理生理学中起着重要作用。为了防止Sah诱导的脑血管痉挛，因此我们在Sah.materials和方法的实验性大鼠模型中使用了盐酸Nebivolol盐酸盐和抗氧化剂：分为对照，Sah，Sah Plus安慰剂，和sah加上痣组。在诱导SAH后开始六小时，每天每天每天口服每天一次盐酸盐酸盐酸盐酸Nebivolol和奈韦洛尔的药物赋形剂，分别为Sah加上萘唑啉和Sah加安慰剂组。在脑切片中测量基底动脉的腔直径和血管壁厚。分析了血清和脑上清液水平（NO）。测量内在抗氧化剂超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-PX）的脑上清液水平作为抗氧化剂状态的标志物。结果：通过不增加水平并通过降低氧化应激来减毒脑血管痉挛。我们的研究还证明，Nebivolol授权逆转SAH通过增加GSH-PX活性相对于SOD.CONCLUSIONS来产生SOD和GSH-PX之间的不平衡：NEBIVOLOL在SAH患者中衰减脑血管痉挛，既不增加水平并降低氧化应激。因此，可以保证将Sah诱导的脑血管痉挛作为抗痉挛和抗氧化剂。

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