Bakirköy Dr. Sadi Konuk Research and Training Hospital, Neurosurgery Clinic, Istanbul, Turkey.
Acta Neurochir (Wien). 2010 May;152(5):855-60. doi: 10.1007/s00701-010-0599-4. Epub 2010 Feb 3.
Cerebral vasospasm (CV) is the leading cause of morbidity and mortality occurring after subarachnoid hemorrhage (SAH). Etiopathogenesis of CV is multifactorial. Selenium is the cofactor of the glutathione peroxidase (GSH-Px) enzyme which is a very important defense mechanism against antioxidants. According to the literature, oxidants are known to play a remarkable role in the pathogenesis of vasospasm occurring after SAH. Therefore, many studies have been conducted with antioxidant agents, based on the theory that elevated activity of GSH-Px enzyme might prevent the development of CV after SAH. Majority of those studies reported positive results. However, as a result of our literature review, we came across no study which involves the investigation of the role of selenium alone in the prevention of CV after SAH. In our study, we aim to find the answer to the following question: "Can selenium alone prevent cerebral vasospasm following SAH at early stage?"
We used the "rat femoral artery vasospasm model" of Okada et al. as the vasospasm model of our study. First, rats were divided into three groups: group 1 (n = 8), control group; group 2 (n = 8), vasospasm group; and group 3 (n = 8), vasospasm + selenium group. Statistical comparison of groups 1 and 2 revealed significant thickening in the vascular wall and a decrease in the lumen diameter in group 2, compared with group 1. Statistical comparison of the vascular lumen diameters of groups 1 and 3 showed no significant difference, whereas the comparison of mean vascular wall thickness displayed a significant increase in group 3. Moreover, statistical comparison of groups 2 and 3 regarding vascular lumen diameters showed a significant decrease in group 2, whereas group 3 displayed a significant decrease in terms of vascular wall thickness.
According to the results of our study, selenium morphometrically prevents the development of peripheral vasospasms.
蛛网膜下腔出血（SAH）后，脑血管痉挛（CV）是发病率和死亡率的主要原因。CV 的病因学是多因素的。硒是谷胱甘肽过氧化物酶（GSH-Px）的辅助因子，GSH-Px 是对抗氧化剂的一个非常重要的防御机制。根据文献，氧化剂在 SAH 后发生的血管痉挛发病机制中起着显著的作用。因此，许多研究都使用抗氧化剂进行了研究，其理论依据是升高的 GSH-Px 酶活性可能预防 SAH 后 CV 的发展。大多数这些研究报告了积极的结果。然而，由于我们对文献的回顾，我们没有发现涉及单独使用硒来预防 SAH 后 CV 的研究。在我们的研究中，我们旨在回答以下问题：“单独使用硒是否可以在早期预防 SAH 后发生脑血管痉挛？”
我们使用冈田等人的“大鼠股动脉血管痉挛模型”作为我们研究的血管痉挛模型。首先，将大鼠分为三组：第 1 组（n = 8），对照组；第 2 组（n = 8），血管痉挛组；第 3 组（n = 8），血管痉挛+硒组。第 1 组和第 2 组的统计学比较显示，与第 1 组相比，第 2 组血管壁明显增厚，管腔直径减小。第 1 组和第 3 组血管腔直径的统计学比较显示无显著差异，而第 3 组平均血管壁厚度的比较显示明显增加。此外，第 2 组和第 3 组血管腔直径的统计学比较显示第 2 组显著减少，而第 3 组血管壁厚度显著减少。
根据我们的研究结果，硒形态学上可预防周围血管痉挛的发展。
