Abstract
To study delayed cerebral vasospasm (DCVS) induced by subarachnoid hemorrhage (SAH), 60 healthy Sprague Dawley (SD) rats were randomly divided into 5 groups (12 rats in each group), namely sham operation group, blood injection model group, nimodipine group, flunarizine hydrochloride group, and normal group. Then, the physiological parameters were detected, and after the rats were killed under anesthesia, the degree of nerve injury, vasospasm as well as the therapeutic effect of drugs were evaluated by Western Blot (WB). Neurological impairment (NI), endothelial contraction and spasm were obvious in rats following blood injection. The expression of Cav3.1 on T-type calcium channels was significantly higher in the blood injection model group than in the sham operation group along with the normal group. Moreover, Cav3.1 mRNA was expressed in all groups. The Cav3.1 expression in blood injection model group and two drug groups were significantly higher than that in sham operation group and lower than that in blood injection model group. Vasospasm was improved in two drug groups, which indicated that calcium channel antagonists nimodipine and flunarizine hydrochloride had a certain therapeutic effect on DCVS in rats. The decrease in body weight and food intake of the two groups of rats treated with drugs decreased, and the delayed vasospasm was improved, but the expression of Cav3.1 was not changed significantly, indicating nimodipine and flunarizine hydrochloride had a therapeutic effect on delayed vasospasm in rats, but Cav3.1 expression on calcium channels was not affected.