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Background/aim: We examined the protective effects of the natural flavonoid, quercetin, against cerebral vasospasm in an experimental rat subarachnoid haemorrhage (SAH) model. Materials and methods: Thirty-eight albino Wistar rats were divided into five groups as follows: group 1 (G1, n=8), no experimental intervention; group 2 (G2, n=8), subarachnoid physiological saline; group 3 (G3, n=8), SAH; group 4 (G4, n=7) SAH and low-dose (10 mg/kg) quercetin treatment; group 5 (G5, n=7), SAH and high-dose (50 mg/kg) quercetin treatment. Subarachnoid haemorrhage was induced by injection of 0.15 cc of autologous blood taken from the tail artery into the cisterna magna from the craniocervical junction and basilar arteries and blood samples were taken for biochemical and histopathological analyses. Results: Malondialdehyde (MDA) levels were significantly higher in G2 and G3 than in G1 (P < 0.05). Significant decreases in MDA were observed in G4 and G5 compared with G2 (P < 0.05, G4-G2; P < 0.05, G5-G2). There were no significant differences between G2 and G3 or among G1, G4, and G5. No statistically significant differences were found in total antioxidant capacity between the groups (P > 0.05). There were no significant differences in basilar artery (BA) wall thickness between G3 and G4 or between G3 and G5, but G4 and G5 showed greater luminal diameters than G3 (P < 0.05). There were no significant differences in BA thickness or luminal diameter between G4 and G5. Conclusion: Our results suggested that quercetin may be beneficial in SAH therapy by preventing vasospasm. [ABSTRACT FROM AUTHOR]

Abstract: We examined the effects of the phosphodiesterase 5 (PDE-5) inhibitor vardenafil on cerebral vasospasm in an experimental rat subarachnoid hemorrhage (SAH) model. Thirty-two albino Wistar rats were divided into five groups: G1, no experimental intervention; G2, administered subarachnoid physiological saline after sham surgery; G3, subjected to SAH; G4, subjected to SAH and administered low-dose (0.5mg/kg) vardenafil treatment; and G5, subjected to SAH and administered high-dose (5mg/kg) vardenafil treatment. For animals in G3, G4 and G5, SAH was induced by an injection of autologous non-heparinized blood into the cisterna magna. Immediately after SAH, for animals in G4 and G5, vardenafil was administered by gavage at intervals of 8 hours for 2days. The rats were then decapitated, and basilar arteries and blood samples were taken for biochemical and histopathological examination. Malonyldialdehyde values in G2 (p =0.004) and G3 (p =0.002) were significantly higher than those in G1. G4 and G5 had significantly lower values than G2 and G3 (p =0.014, G4 v. G2; p =0.005, G4 v. G3; p =0.005, G5 v. G2; p =0.002, G5 v. G3). Total antioxidant capacity (TAC) values in G3 were significantly lower than those in G1 (p =0.041). TAC values in G4 and G5 were significantly higher than those in G3 (p =0.043). Mean luminal diameter in G3 was significantly smaller compared with G1 and G2 (p =0.002), but larger in G4 (p =0.002) and G5 (p =0.001) compared with G3. Mean luminal diameter was also significantly larger in G5 than in G2 (p =0.008) and G4 (p =0.038). Mean wall thickness in G2 (p =0.015) and G3 (p =0.002) was significantly thicker compared with G1. Wall thickness was significantly thinner in G4 and G5 compared with G2 and G3 (p =0.008, G4 v. G2; p =0.001, G4 v. G3; p =0.005, G5 v. G2; p =0.001, G5 v. G3). Our results confirm that vardenafil may induce vasodilatation and provide potential benefits in SAH therapy by preventing vasospasm. [Copyright &y& Elsevier]

Abstract: We investigated the effect of two different doses of dexmedetomidine on vasospasm in a rat model of subarachnoid haemorrhage (SAH). SAH was induced by injecting 0.3mL blood into the cisterna magna in all rat groups except the control (Group C). At 1 hour and 24 hours after SAH, 5μg/kg dexmedetomidine was given to group D5, and 10μg/kg dexmedetomidine was given to group D10. No medication was administered to the haemorrhage group (Group H). Malondialdehyde (MDA) and paraoxonase (PON) levels were measured at 48 hours after SAH. Mean wall thickness (MWT), mean luminal diameter (MLD), and proliferating cell nuclear antigen (PCNA) expression of the basilar artery were evaluated. MDA levels and MWT were lower in the dexmedetomidine groups. The lowest MDA levels and MWT were found in Group D10. The MLD was lowest in Group H. PCNA expression was observed only in Group D10. We concluded that dexmedetomidine reduces oxidative stress and vasospasm following SAH in a dose-dependent manner. [Copyright &y& Elsevier]

Abstract: We investigated the effect of ebselen relative to nimodipine in an animal model of subarachnoid hemorrhage. Thirty Wistar albino rats were divided into 5 groups: G1, no intervention; G2, sham surgery without subarachnoid hemorrhage (SAH); G3, SAH only; G4, SAH plus nimodipine treatment; G5, SAH plus ebselen treatment. For G2 animals, physiological saline (0.9% NaCl) was injected into the cisterna magna. For G3, G4 and G5 animals, SAH was induced by injecting autologous non-heparinized blood into the cisterna magna. One hour after injection, G4 animals received nimodipine at 6-hour intervals and G5 animals received ebselen twice a day for 48hours. After treatment, brain tissue and blood samples were taken for biochemical and histopathological examination. Mean malonyldialdehyde concentration was significantly higher in G3 than in G1 (p <0.0001), G2 (p =0.01), G4 (p =0.002) and G5 (p =0.014), and significantly higher in G5 than in G1 (p =0.013). Mean superoxide dismutase activity was significantly lower in G4 than in both G1 (p =0.025) and G2 (p =0.02). Mean wall thickness was significantly greater in G3 than in G1 (p <0.0001), G2 (p =0.01), G4 (p <0.0001) and G5 (p <0.0001). Mean wall thickness was also significantly greater in both G1 and G2 than in G4 (p <0.0014 and p <0.0001) and G5 (p <0.0001 and p <0.0001). Mean luminal diameter of the basilar artery was significantly smaller in G3 than in G2 (p =0.02), G4 (p <0.018) and G5 (p <0.001). Our results confirm that ebselen may have neuroprotective effects by acting to prevent vasospasm. [Copyright &y& Elsevier]

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. [ABSTRACT FROM AUTHOR]