OBJECTIVE: We examined the protective effects of hesperidin on cerebral 
vasospasm by establishing an experimental rat model of subarachnoid hemorrhage 
and performing biochemical, pathologic, and histomorphometric analysis on these 
data.
METHODS: Forty albino Wistar rats were randomly divided into 5 groups of n = 8 
in each: group (G)1, no experimental interventions; G2, subjected to 
subarachnoid hemorrhage; G3, subjected to subarachnoid hemorrhage and 
administered saline (100 mg/kg); G4, subjected to subarachnoid hemorrhage and 
treated with low-dose hesperidin (50 mg/kg); and G5, subjected to subarachnoid 
hemorrhage and treated with high-dose hesperidin (100 mg/kg). Subarachnoid 
hemorrhage was created by injecting 0.15 cc of autologous blood taken from the 
rat-tail artery and injected into the cisterna magna from the craniocervical 
junction. Drugs were administered intraperitoneally as twice daily doses for 48 
hours. Rats were euthanized at the end of this period.
RESULTS: No statistically significant decrease was observed in malondialdehyde 
levels, which is the end-product of lipid peroxidation, among the drug groups 
(G4 and G5). Thin sections prepared from the basilar artery were examined 
morphologically. Severe luminal narrowing and vessel-wall thickening were 
observed in the subarachnoid hemorrhage groups (G2, G3). In the 
hesperidin-administered groups (G4, G5), it was determined that vessel wall 
thickness measurements revealed thinner walls than in the subarachnoid 
hemorrhage groups (G2, G3) and the luminal diameters were significantly larger 
than in the subarachnoid hemorrhage groups (G2, G3).
CONCLUSIONS: These findings suggest that hesperidin has no effect on 
malondialdehyde-associated lipid-peroxidation activity; however, it might be 
useful in subarachnoid hemorrhage therapy because of its beneficial effects on 
vessel wall thickness and luminal diameters.