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    The effect of dexmedetomidine in the prefrontal cortex of rabbits after subarachnoidal hemorrhage
    (UNIVERSITATSVERLAG ULM GMBH, 2006) Eser, Olcay; Cosar, Murat; Fidan, Huseyin; Sahin, Onder; BuyukbaS, Sadik; Ela, Yuksel; Songur, Ahmet
    Background: This study was undertaken to examine the possible neuroprotective effect of dexmedetomidine in the prefrontal cortex of vasospastic subarachnoid hemorrhage (SAH) rabbits. Materials and Methods: Experimental SAH was performed to the 12 of 18 New Zealand rabbits by injecting 0.9 ml of autologous arterial blood/1 kg of body weight to cisterna magna. Craniotomy procedure was performed to the rest 6 rabbits (control group) (Group A) except performing experimental SAH. Forty eight hours after SAH was established, 5 mL/kg/hour 0.9% sodium chloride were infused to the SAH-alone group (n=6) (Group B) and 5 mu g/kg/h dexmedetomidine were infused to the SAH-dexmedetomidine group (n=6) (Group C) for 2 hours. Rabbits of all groups were sacrificed via penthotal after 24 hours following this drug administration processes. Brains were removed from the skull totally, prefrontal cortices were blocked from the right hemisphere for histopathological study, and prefrontal cortex of left hemispheres were dissected for biochemical analyses. So, malondialdehyde levels, activities of xantine oxidase, and superoxide dismutase were studied from the left prefrontal cortex. Results: The histopathological results showed that dexmedetomidine has neuroprotective effect in SAH induced prefrontal cortex injuries. The antioxidant parameters also supported the neuroprotective effect of dexmedetomidine. Conclusion: The present study showed the neuroprotective effect of dexmedetomidine in the prefrontal cortex of rabbits after vasospastic subarachnoid hemorrhage.
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    The influence of dexmedetomidine on ischemic rat hippocampus
    (ELSEVIER SCIENCE BV, 2008) Eser, Olcay; Fidan, Huseyin; Sahin, Onder; Cosar, Murat; Yaman, Mehmet; Mollaoglu, Hakan; Songur, Ahmet
    In our study, we evaluated the neuroprotective effects of dexmedetomidine on oxidantantioxidant systems, pro -inflammatory cytokine TNF-a and number of apoptotic neurons on hippocampus and dentate gyrus after transient global cerebral I/R injury. Eighteen rats divided into 3 groups, equally. Group I rats were used as shams. For group II and III rats, they were prepared for transient global cerebral ischemia using a four-vessel- occlusion model. 5 mL/kg/h 0.9% sodium chloride was infused to the Group II and 3 Pg/kg/h/5 ml dexmedetomidine was infused to the Group III for 2 h after I/R injury. The levels of MDA and NO and activities of SOD and CAT were measured in the left hippocampus tissue. The levels of TNF-a concentration were measured in the plasma. The number of apoptotic neurons was counted by TUNNEL method in histological samples of right hippocampus tissue. MDA and NO levels increased in Group II compared with Group I rats (p=0.002, p=0.002, respectively). In group III, MDA and NO levels decreased as compared to Group 11 (p=0.015, p=0.002, respectively). SOD and CAT activities increased in Group III as compared to Group II rats (p = 0.002, p = 0.002, respectively). The decrease in TNF-a levels of group III was significant as compared to group II (p=0.016). The number of apoptotic neurons in group III was lower than Group II rats. Our study showed that dexinedetomidine has a neuroprotective effect on hippocampus and dentate gyrus of rats after transient global cerebral I/R injury. (c) 2008 Elsevier B.V. All rights reserved.
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    The neuroprotective effect of dexmedetomidine in the hippocampus of rabbits after subarachnoid hemorrhage
    (ELSEVIER SCIENCE INC, 2009) Cosar, Murat; Eser, Olcay; Fidan, Huseyin; Sahin, Onder; Buyukbas, Sadik; Ela, Yuksel; Yagmurca, Murat
    Background: Subarachnoid hemorrhage is a Serious Condition. often accompanied by cerebral vasospasm. which may lead to brain ischemia and neurologic deterioration. We evaluated if dexmedetomidine has neuroprotective effects in the hippocampus of vasospastic SAH rabbits or not. Materials and Methods: Eighteen New Zealand rabbits were taken. Ail experimental SAH model was Formed by injecting 0.9 mL of autologous arterial blood per 1 kg of body weight to the cisterna magna of 12 rabbits. Craniotomy was performed ill the control group (n = 6) except performing experimental SAH. Rabbits in the SAH-alone (n = 6) group were infused with 5 mL . kg(-1) . h(-1) 0.9% sodium chloride, and rabbits (n = 6) in the SAH-dexmedetomidine group were infused with 5 mu g . kg(-1) . h(-1) dexmedetomidine for 2 hours, 48 hours alter SAH was established. Rabbits of all groups were sacrificed via penthotal 24 hours after dexmedetomidine administration. Brains were removed immediately. and hippocampal tissues were blocked from the right hemisphere for histopathologic study. In addition to this, hippocampal tissues of left hemispheres were dissected for biochemical analyses to evaluate MDA levels, activity of XO, and SOD. Results: The histopathologic study showed that dexmedetomidine may have a neuroprotective effect in SAH-induced hippocampal injuries. The biochemical parameters Support the neuroprotective effect of dexmedetomidine (P < .05). Conclusion: Our Study showed that dexmedetomidine may have a neuroprotective effect ill the hippocampus of vasospastic SAH rabbits. (C) 2009 Elsevier Inc. All rights reserved.
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    The protective effect of avocado soybean unsaponifilables on brain ischemia/reperfusion injury in rat prefrontal cortex
    (TAYLOR & FRANCIS LTD, 2011) Eser, Olcay; Songur, Ahmet; Yaman, Mehmet; Cosar, Murat; Fidan, Huseyin; Sahin, Onder; Mollaoglu, Hakan
    Object. We investigated the protective effects of avocado/soybean unsaponifiables (ASU) on the prefrontal cortex (PFC) after global brain ischemia/reperfusion (I/R) injury in rats. Methods. Rats were randomly divided into three experimental groups as follows: Group I was control rats, Group II was ischemia rats, Group III was Isch+ASU rats. Brain ischemia was produced via four-vessel occlusion model. These processes followed by reperfusion for 30 min for both II and III groups. Rats were sacrificed and their brains were removed immediately. Malondialdehyde (MDA) and superoxide dismutase (SOD) were measured in left PFC, levels of TNF-alpha concentration were measured in the plasma. The number of apoptotic neurons was assayed in histological samples of the right PFC. Results. MDA and TNF-alpha levels as well as the number of apoptotic neurons were observed to have decreased significantly in Group III compared to Group II, while SOD activities have been found to have increased significantly in Group III in comparison to Group II, significantly. Conclusions. We think that ASU might have an antioxidant and neuroprotective effects in brain I/R injured rats.