Mete, MÖzer, FDDuransoy, YKKocaman, ÜOran, IDemirtas, ESelçuki, M2024-07-182024-07-181302-1664http://akademikarsiv.cbu.edu.tr:4000/handle/123456789/9796Purpose: Cerebral vasospasm is the leading cause of morbidity and mortality following subarachnoid hemorrhage. Although a number of factors have been examined in clinical and experimental studies, the agent(s) responsible for developing and diminishing vasospasm remain poorly understood. Here, the role of edaravone, an antioxidant agent, was evaluated for its ability to diminish vasospasm in an animal model of subarachnoid hemorrhage. Materials and Methods: A rat basilar artery subarachnoid hemorrhage model was used. Rats were divided into three groups: sham (n=7; Group 1), subarachnoid hemorrhage (n=7 Group 2), and subarachnoid hemorrhage plus edaravone (4 mg/kg intraperitoneally, n=7; Group 3). At the end of the seventh day, the rats were sacrificed, their brains were removed, and sections were taken from the basilar artery. These were examined using a light microscope, comparing the internal luminal circumference of the basilar artery of each group. Results: The circumference was largest in Group 1, followed by Group 3 and then Group 2. That of Group 3 was 2% higher than that of Group 2, but this difference was not statistically significant. Conclusion: This animal model for vasospasm suggests that edaravone helps enlarge internal luminal circumference following vasospasm caused by subarachnoid hemorrhage. It may do this by blocking lipid peroxidation and thereby reducing the effects of oxyhemoglobin and reactive oxygen species.EnglishFREE-RADICAL SCAVENGERCEREBRAL VASOSPASMISCHEMIAINJURYDEFICITSDAMAGEArticle