BACKGROUND: 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?" METHODS: 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. CONCLUSION: According to the results of our study, selenium morphometrically prevents the development of peripheral vasospasms.
BACKGROUND: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?" METHODS: 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. CONCLUSION: According to the results of our study, selenium morphometrically prevents the development of peripheral vasospasms.