Yazar "Cosar, Murat" seçeneğine göre listele
Listeleniyor 1 - 8 / 8
Sayfa Başına Sonuç
Sıralama seçenekleri
Öğe Brain tissue biochemical parameters in cerebral ischemic reperfusion injury after hemorrhagic shock: An experimental study(UNIVERSITATSVERLAG ULM GMBH, 2007) Cosar, Murat; Eser, Olcay; Fidan, Hueseyin; Kalkan, Erdal; Buyukbas, Sadik; Ozen, O. A.Objective: In this study, we showed the tissue biochemical parameters in cerebral ischemic reperfusion injury that developed after hemorrhagic shock in a rat model. Materials and Methods: Hemorrhagic shock models were established in 36 adult Sprague-Dawley rats and divided into six groups: control (group A), hemorrhagic shock (HS) (group B), first hour ischemic reperfusion (IR+1h) (group Q, 311 hour IR (IR+3h) (group D), 61(th) hour IR (IR+6h) (group E) and 2411 hour IR (IR+24h) (group F). The rats were sacrificed by bleeding from the intracardiac area after finishing the experiment. The brains were removed from the skull immediately. Bilateral hemispheres were dissected for biochemical analyses, and activities of superoxide dismutase (SOD) and myeloperoxidase (MPO), and the levels of malondialdehyde (MDA) were evaluated. Results: The study revealed that the SOD activities decreased stepwise from group A (control) to group F (IR+24h) (P<0.05). In addition, MDA levels and MPO activities increased stepwise from group A (control) to group F (IR+24h). Conclusion: We think that the level of cell injury increases stepwise in the first, 3(rd), 6(th) and 24(th) hours after ischemia reperfusion injury.Öğe Does Botox effect neural tube development in early chick embryos?(SPRINGER, 2007) Eser, Olcay; Yaman, Mehmet; Cosar, Emine; Konak, Abdullah; Cosar, Murat; Sahin, Oender; Gueney, OenderBotulinum toxin (BTX) is a potent neurotoxin produced by Clostridium botulinum and has wide usage in different areas. The current study aimed to analyze the effects of C. botulinum toxin on the central nerve system in chick embryos. Forty fertile Hubbard Broil eggs, all at Stage 8 of development, were divided into four equal groups: Group 1 embryos (n=10), the control group, were explanted and grown for 18 h in a nutrient medium (thin albumin). Group 2 embryos (n=10) were grown in medium containing 5 U BTX, Group 3 embryos (n=10) in a medium containing 10 U BTX and Group 4 embryos (n=10) in medium containing 20 U BTX. After the incubation period, 80% of Group 1 and 2 embryos and 90% of Group 3 and 4 embryos had intact neural tubes (P > 0.05). The results of this study suggest that BTX had no additional effect on neural tube development in early chick embryos.Öğe The effect of aprotinin on brain ischemic-reperfusion injury after hemorrhagic shock in rats: An experimental study(LIPPINCOTT WILLIAMS & WILKINS, 2007) Eser, Cay; Kalkan, Erdal; Cosar, Murat; Buyukbas, Sadik; Avunduk, Mustafa Cihat; Aslan, Adem; Kocabas, VolkanBackground. We aimed to demonstrate the positive effects of the serine protease inhibitor aprotinin on neural ischemia-reperfusion injury and apoptosis in a rat model. Methods: There were 18 rats divided into 3 groups: group A (sham, n = 6), group B (ischemia-reperfusion, n = 6), and group C (ischemia-reperfusion + aprotinin, n = 6). The systolic blood pressure of the group B and C rats was decreased to 40% to 50% of the normal level by taking blood from the femoral vein to develop hemorrhagic shock. The blood was retained and given to the remaining group B and C rats for reperfusion 20 minutes after the procedure. In group B, isotonic solution and, in group C, aprotinin was administered to the rats 5 minutes before reperfusion. After the rats were killed, the brain tissue samples were fixed for histopathologic examination. Brain tissue superoxide dismutase, malondialdehyde, and tissue myeloperoxidase level and apoptotic cell analyses were performed in all groups. Results: Superoxide dismutase level decreased from group A to group B and increased from group B to group C (p < 0.05). Malondialdehyde and myeloperoxidase levels and apoptotic cells increased from group A to group B and decreased from group B to group C (p < 0.05). Conclusions: The results suggest that the systemic use of aprotinin in ischemic neural tissue prevents reperfusion injury and also protects the morphologic, functional, and biochemical integrity of the neural tissue.Öğe 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, AhmetBackground: 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.Öğe The evaluation of protective effects of FK-506 on neural ischemic-reperfusion injury: an experimental study(SPRINGER HEIDELBERG, 2007) Eser, Olcay; Kalkan, Erdal; Cosar, Murat; Yaman, Mehmet; Buyukbas, Sadik; Avunduk, Mustafa Cihat; Fidan, HueseyinObjective: In this study, we aimed to delineate the mode of neuroprotective action of FK-506, and demonstrated that FK-506 could decrease oxidative stress and apoptotic cell death in an in vivo rat model of neural ischemia-reperfusion after hemorrhagic shock. Methods: Thirty rats were used as experimental subjects and divided into five equal groups. Group A rats (sham group, n = 6) were anesthetized and craniotomies were performed for collecting brain tissue samples. In group B ischemia-reperfusion (I/R + 1 h, n = 6), group C (I/R + 24 h, n = 6), group D (I/R + 1 h FK-506, n = 6) and group E (I/R + 24 h FK-506, n = 6), systolic blood pressure of the rats decreased to 40-50% of the normal level via bleeding from the femoral vein. Thus, a hemorrhagic shock and ischemic neural tissue model was formed. The blood was retained and given to the remaining animals in groups B, C, D and E via femoral vein for reperfusion 20 min after the procedure. In group D and E, 1 mg/kg FK-506 in 0.5 ml isotonic solution was administered to the rats 5 min before reperfusion. Group B and D rats were sacrificed after 1 hand group C and E rats were sacrificed 24 h after reperfusion; the rats were sacrificed via bleeding associated with intracardiac puncture. Craniotomy was also performed in groups B, C, D and E and brain tissue samples were fixed using neutral buffered 10% formaldehyde solution for immunohistopathological examination as in group A. Brain tissue superoxide dismutase (SOD) activities, malondialdehyde (MDA) levels, tissue myeloperoxydase (MPO) activities and apoptotic cell analyses with APO 2.7 immunohistochemically were also performed in all groups. Results: The result of the study revealed that the SOD activities were lower for groups B (I/R + 1 h) and C (I/ R + 24 h) than for group A (sham group) (p < 0.05). In addition, SOD activities were higher in groups D (I/ R + 1 h FK-506) and E (I/R + 24 h FK-506) than in groups B (I/R + 1 h) and C (I/R + 24 h) (p < 0.05). MDA levels, MPO activities and the number of apoptotic cells were lower in group A (sham group) than in groups B (I/R + 1 h) and C (I/R + 24 h) (p < 0.05). In addition to these MDA levels, MPO activities and the number of apoptotic cells were higher in groups B (I/R + 1 h) and C (I/R + 24 h) as compared to groups D (I/R + 1 h FK-506) and E (I/R + 24 h FK-506) (p < 0.05). Conclusion: The results suggest that the prophylactic use of FK-506 in an in situ ischemic neural tissue may prevent reperfusion injury.Öğe 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, AhmetIn 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.Öğe 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, MuratBackground: 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.Öğe 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, HakanObject. 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.
