Aydogmus E. | Gul S. | Bahadir B.

Article | 2019 | World Neurosurgery122

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. © 2018 Elsevier Inc Daha fazlası Daha az

Ayoglu H. | Gul S. | Hanci V. | Bahadir B. | Bektas S. | Mungan A.G. | Turan I.O.

Article | 2010 | Journal of Clinical Neuroscience17 ( 6 ) , pp.770 - 773

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 0.3 mL blood into the cisterna magna in all rat groups except the control (Group C). At 1 hour and 24 hours after SAH, 5 µg/kg dexmedetomidine was given to group D5, and 10 µg/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) exp . . .ression 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. © 2009 Elsevier Ltd. All rights reserved Daha fazlası Daha az

Gul S. | Bahadir B. | Hanci V. | Bektas S. | Can M. | Kalayci M. | Acikgoz S.

Article | 2010 | Journal of Clinical Neuroscience17 ( 8 ) , pp.1038 - 1041

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 (0.5 mg/kg) vardenafil treatment; and G5, subjected to SAH and administered high-dose (5 mg/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. Im . . .mediately after SAH, for animals in G4 and G5, vardenafil was administered by gavage at intervals of 8 hours for 2 days. 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. © 2010 Elsevier Ltd. All rights reserved Daha fazlası Daha az

Gul S. | Bahadir B. | Hanci V. | Acikgoz S. | Bektas S. | Ugurbas E. | Ankarali H.

Article | 2010 | Journal of Clinical Neuroscience17 ( 5 ) , pp.608 - 611

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 da . . .y for 48 hours. 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. © 2009 Elsevier Ltd. All rights reserved Daha fazlası Daha az