Abstract: [Abstract] Objective · To observe the degree of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) at different time poininvestigate the effects of ethyl pyruvate (EP) on CVS following SAH and its mechanism. Methods · Fifty healthy SD rats were randomly difive groups i.e. sham group, SAH-3 d group, SAH-5 d group, SAH-7 d group and SAH-9 d group (n=10 in each group). Sham group was built cisternal injection with 0.3 mL saline each time, and SAH group was built by double cisternal injection with 0.3 mL autologous blood each neurological function and degree of CVS were observed. Another forty-eight healthy SD rats were randomly divided into three groups i.e. sh(equal volume) group, SAH+saline (equal volume) group and SAH+EP [100 mg/(kg·d)] group (n=16 in each group). The neurological functionCVS and cell apoptosis of basilar artery were observed on day 7. The expressions of p-Akt, Bax, Bcl-2 and cleaved caspase-3 were also observed Results · CVS significantly increased on day 3, decreased on day 5, and then significantly increased to top level on day 7, and gradually decreased Compared with sham+saline group, the neurological scores were significantly decreased in SAH+saline group on day 7. Compared with sham+saCVS and cell apoptosis of basilar artery were significantly increased in SAH+saline group on day 7. Compared with sham+saline group, the eof Bax and cleaved caspase-3 were significantly up-regulated, while the expressions of p-Akt and Bcl-2 were significantly down-regulated in SAgroup on day 7. Compared with SAH+saline group, the neurological scores significantly increased in SAH+EP group on day 7. Compared with Sgroup, CVS and cell apoptosis of basilar artery significantly decreased in SAH+EP group on day 7. Compared with SAH+saline group, the exprBax and cleaved caspase-3 were significantly down-regulated, while the expressions of p-Akt and Bcl-2 were significantly up-regulated in SAH+EP day 7. Conclusion · The double hemorrhage model rat has most severely CVS on day 7. EP can attenuate vasospasm after SAH, and its mechanisassociated with inhibition of cell apoptosis. PI3K/Akt signaling pathway may be involved, which may provide a novel therapeutic target for CVS.

Key words: ethyl pyruvate, subarachnoid hemorrhage, cerebral vasospasm, cell apoptosis