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  1. Ana Sayfa
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Yazar "Ozturk, Levent" seçeneğine göre listele

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    Dexmedetomidine protects against lipid peroxidation and erythrocyte deformability alterations in experimental hepatic ischemia reperfusion injury
    (Taylor & Francis Ltd, 2012) Arslan, Mustafa; Comu, Faruk Metin; Kucuk, Aysegul; Ozturk, Levent; Yaylak, Faik
    Background: Hepatic ischemia-reperfusion injury is a common clinical problem in hepatic surgery and transplantation. Several cellular and tissue structural and functional alterations are observed in such injury. The aim of this study was to evaluate the effect of dexmedetomidine on lipid peroxidation and erythrocyte deformability during ischemia-reperfusion injury in rats. Methods: Twenty-four Wistar Albino rats were randomly separated into three groups as control (C), ischemia-reperfusion injury (I/R) and dexmedetomidine group (I/R-D). Ischemia was induced with portal clampage for 45 min and reperfusion period was 45 min after declampage. Group I/R-D received dexmedetomidine 100 mu g/kg i.p. 30 min before portal clampage. Serum malondialdehyde and superoxide dismutase activities to document lipid peroxidation and erythrocyte deformability index were investigated. Results: Serum superoxide dismutase and malondialdehyde activity levels were significantly higher and erythrocyte deformability index was decreased in hepatic ischemia-reperfusion group. However, these changes were observed to be prevented with dexmedetomidine treatment when given before portal clampage. Conclusion: These findings clearly indicate that erythrocyte deformability index is decreased in hepatic ischemia reperfusion injury and has a potential role to prevent these alterations. The protective effect of dexmedetomidine on hepatic I/R injury is also decreased lipid peroxidation. Further experimental and clinical investigations may clarify the molecular mechanisms and clinical significance of these findings.
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    Effect of dexmedetomidine on ischemia-reperfusion injury of liver and kidney tissues in experimental diabetes and hepatic ischemia-reperfusion injury induced rats
    (Anaesthesia Pain & Intensive Care, 2016) Sezen, Saban Cem; Isik, Berrin; Bilge, Mustafa; Arslan, Mustafa; Comu, Faruk Metin; Ozturk, Levent; Kavutcu, Mustafa
    Background: Reperfusion following ischemia can lead to more injuries than ischemia itself especially in diabetic patients. The aim of this study was to evaluate the effect of dexmedetomidine on ischemia-reperfusion injury (IRI) in rats with have hepatic IRI and diabetes mellitus. Methodology: Twenty-eight Wistar Albino rats were randomised into four groups as control (C), diabetic (DC), diabetic with hepatic ischemia-reperfusion injury (DIR), and diabetic but administered dexmedetomidine followed by hepatic IRI (DIRD) groups. Hepatic tissue samples were evaluated histopathologically by semiquantitative methods. Malondialdehyde (MDA), superoxide dismutase (SOD), glutathion s-transpherase (GST), and catalase (CAT) enzyme levels were investigated in liver and kidney tissues as oxidative state parameters. Results: In Group DIR; hepatocyte degeneration, sinusoidal dilatation, pycnotic nucleus, and necrotic cells were found to be more in rat hepatic tissue; while mononuclear cell infiltration was higher in the parenchyme. MDA levels were significantly lower; but SOD levels were significantly higher in Group DIRD with regard to Group DIR. In the IRI induced diabetic rats' hepatic and nephrotic tissues MDA levels, showing oxidative injury, were found to be lower. SOD levels, showing early antioxidant activity, were higher. Conclusion: The enzymatic findings of our study together with the hepatic histopathology indicate that dexmedetomidine has a potential role to decrease IRI.
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    Effect of different doses of pregabalin on erythrocyte deformability in rats with lower limb ischemia reperfusion injury
    (Anaesthesia Pain & Intensive Care, 2017) Ozer, Abdullah; Comu, Faruk Metin; Demirtas, Huseyin; Kilic, Yigit; Mardin, Baris; Ozturk, Levent; Kucuk, Aysegul
    Background & Objective: Acute ischemia reperfusion (IR) injury observed in the lower extremities occurs especially when a temporary cross-clamp is applied to the abdominal aorta during aortic surgery. Preoperative pregabalin has been used as a part of multimodal analgesia in postoperative pain treatment in recent years. Pregabalin has become one of the increasingly common agents in postoperative analgesia. In this study, we aimed to investigate the effect of pregabalin on erythrocyte deformability in rats undergoing IR. Methodology: 24 male Wistar albino rats weighing between 200-250 g were used in the study. Rats were randomly divided into 4 groups of 6 rats each (Control, Ischemia-Reperfusion (IR), IR-Pregabalin 50 mg (50 mg/kg), IR-Pregabalin 200 mg (200 mg/kg). Pregabalin was administered intraperitoneally 30 min before the procedure. An atraumatic microvascular clamp was placed across the infrarenal abdominal aorta in the IR groups. Following 120 min of ischemia, the clamp was removed and reperfusion was continued for 120 min. All rats were euthanized by intraperitoneal administration of ketamine (100 mg/kg) and taking blood from the abdominal aorta. Erythrocytes were seperated from heparinized whole blood samples. Deformability measurements were made in erythrocyte suspensions in phosphate buffered saline. A constant flow filtrometer system was used to measure erythrocyte deformability and relative resistance was calculated. Results: It was found that the formation of ischemia reperfusion increases the relative resistance according to the control group (p < 0.0001). It was determined that application of pregabalin 50 or 200 mg did not change erythrocyte deformability in ischemia reperfusion-induced rats (p = 0.632, p = 0.811). Conclusion: The administration of 50 or 200 mg of pregabalin has no negative effect on the erythrocyte deformability in ischemia reperfusion-induced rats. We think that pregabalin can be safely used for analgesia in the cases of IR. However, these findings should be supported by clinical and experimental studies carried out in more detailed and broader series.
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    Investigation of Effects of Propofol and Vitamin C Administration on Hepatic and Renal Tissue in Diabetic Rats
    (Gazi Univ, Fac Med, 2015) Arslan, Mustafa; Bilge, Mustafa; Sezen, Saban Cem; Ozturk, Levent; Isik, Berrin; Comu, Faruk Metin; Yilmaz, Dervis
    Obective: A close relationship between diabetic complications and lipid peroxidation is known. It was shown that in diabetic rat pharmacodynamics and pharmacokinetics of propofol was changed. We aim to investigate effects of application propofol and vitamin C on liver and kidney tissue in diabetic rats. Method: Twenty eight wistar albino rats were randomly divided into 4 study groups. Rats in control group were treated only with saline intra peritonealy. Experimental diabetes was induced with a single dose of streptozotocin (60 mg/kg). In propofol adminastrated diabetic rat group (DP) 150 mg/kg propofol was given intraperitoneally. In both propofol and vitamin C adminastrated rats group (DP+Vit C), 100 mg/kg vitamin C was given before 30 minutes administration of 150 mg/kg propofol. In the diabetic control group (DC) administartion of intraperitoneally saline solution alone to the diabetic rats was achieved. Rats were sacrified and liver and kidney tissue were removed. Liver and renal tissue was obtained for histological and biochemical determination. Antioxidant enzymes SOD, CAT, GST activities and MDA concentration were determined in liver and renal tissue. Results: Liver MDA levels in group DC was found to be significantly higher than DP, DP+Vit C and C groups (p=0.024, p=0.008, p=0.016). Liver SOD activity in group 3 was found to be significantly lower in groups DP+Vit C and C (p=0.011, p=0.038). Liver GST activity in group DP+Vit C was found to be significantly lower when compared with group C (p = 0.011). Liver CAT activity showed no difference among groups. Renal MDA levels in group DC was found to be significantly higher in groups DP+Vit C and C (p=0.016, p=0.010). Renal SOD activity in DC was found to be significantly lower than groups DP, DP+Vit C and C (p=0.028, p=0.019, p=0.009). Renal GST and CAT activity showed no difference among groups. Histopathalogically group DP was more damaged than in group C. Conclusion: Diabetes increased lipid peroxidation and reduced the antioxidant activity. However, application of vitamin C reduced lipid peroxidation and increased antioxidant activity. Results of our study have to be supported other experimental studies.

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