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    Effects of intravenous ibuprofen and lornoxicam on erythrocyte deformability in rats undergoing hind limb ischemia reperfusion injury
    (Comenius Univ, 2016) Sivgin, V; Kucuk, A.; Comu, F. M.; Kosem, B.; Kartal, S.; Turgut, H. C.; Alkan, M.
    BACKGROUNDAND AIM: Acute hind limb ischemia reperfusion (I/R) injury is a common consequence of abdominal aorta cross-clamping during aortic surgery. Erythrocyte deformability is affected by I/R process and may lead to increased tissue and organ injury. Lornoxicam and intravenous ibuprofen are becoming commonly used as non-steroidal anti-inflammatory drugs (NSAID) for postoperative analgesia. In this study, we aimed to investigate the effects of lornoxicam (2 mg/kg iv) and intravenous ibuprofen (30 mg/kg iv) on erythrocyte deformability in I/R model in rats. MATERIALS AND METHODS: Four study groups, each containing 6 Wistar rats were created. Laparotomy was performed in all groups under general anesthesia with ketamine and xylazine. In all groups except sham group, ischemia and reperfusion were achieved by clamping and declamping the infrarenal abdominal aorta for 120 minutes. Rats in Group IR+L received intravenous infusion of lornoxicam (2 mg/kg) while rats in Group 1R+I received intravenous infusion of ibubrofen (30 mg/kg) following 2 hours of ischemic period. At the end of reperfusion period, erythrocyte packs were prepared from heparinized blood samples. Erythrocyte suspensions with hematocrit at a concentration of 5% in a phosphate-buffered saline (PBS) were used in order to perform deformability measurements. The value of p<0.05 was considered statistically significant. RESULTS: Relative resistance has increased in ischemia reperfusion group when compared to control group (p < 0.0001). Lornoxicam or ibuprofen intravenous treatments did not change the erythrocyte deformability during ischemia reperfusion period in rats (p=0.851, p=0.690). CONCLUSION: Intravenous ibuprofen or lornoxicam administrations during ischemia reperfusion period in rats have no negative effect on erythrocyte deformability. The findings of the study should be supported with more detailed and extensive clinical/experimental studies in the future (Fig. 1, Ref. 18). Text in PDF www.elis.sk.
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    The effects of low and high doses of sugammadex on kidney tissue in streptozotocin-induced diabetic rats
    (Comenius Univ, 2015) Kip, G.; Turgut, H. C.; Alkan, M.; Aydin, M. E.; Erbatur, M. E.; Kiraz, H. A.; Unal, Y.
    BACKGROUND: Sugammadex is primarily excreted via renal route. We investigated effects of low and high doses of sugammadex (16 mg/kg versus 96 mg/kg) on renal tissue samples of streptozotocin-induced diabetic rats. MATERIAL AND METHODS: Twenty-four Wistar albino rats were divided into 4 groups. Group C (control - 0.9 % NaCl), Group DC (diabetes control; 55 mg/kg streptozotocin, IP, only), Group DR-16S (diabetes-rocuronium - 16 mg sugamnnadex, IV.) and Group DR-96S (diabetes- rocuronium - 96 mg sugammadex, IV). Renal tissue histopathological evaluation and antioxidant status (measurements of MDA levels and NO activities) were studied. RESULTS: Significantly higher levels of all inflammation parameters (inflammation, degeneration/necrosis, tubular dilatation, tubular cell degeneration, dilatation in Bowman's space, tubular hyaline casts, and lymphocyte infiltration) were found in the 96 mg/kg sugammadex group. Higher MDA tissue levels and lower NO activity were found in the 96 mg/kg sugammadex group. DISCUSSION: We can conclude that high-dose (96 mg/kg) sugammadex administration resulted in significant renal tissue damage in diabetic rats. As a consequence, low doses of sugamnnadex have to be preferred in diabetic patients (Tab. 2, Fig. 4, Ref. 26). Text in PDF www.elis.sk.
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    Vitamin C ameliorates high dose Dexmedetomidine induced liver injury
    (Comenius Univ, 2016) Arslan, M.; Sezen, S. C.; Turgut, H. C.; Kocabiyik, M.; Arpaci, H.; Comu, F. M.; Kavutcu, M.
    BACKGROUND: We investigated whether vitamin C has protective effects on rat liver tissue treated with different dexmedetomidine doses. MATERIAL AND METHODS: Thirty five wistar albino rats were randomly divided into 5 groups (Control (0.9 % NaCI intraperitoneally (ip), Dexmedetomidine 5 mu g.kg(-1) (ip), Dexmedetomidine 5 mu g.kg(-1) ip plus Vitamin C (100 mng.kg(-1)), Dexmedetomidine 10 mu g.kg(-1) ip and Dexmedetomidine 10 mu g.kg(-1) ip plus Vitamin C (100 mg.kg-1). Histopathological liver injury, superoxide dismutase (SOD) activity and tissue Malondialdehyde levels were investigated. RESULTS: Hepatocyte degeneration was significantly higher in D10 group than those in other study groups (p < 0.0001, p = 0.002, p < 0.0001, p = 0.005, respectively). Similarly, liver tissue sinusoidal dilatation and hepatocyte necrosis were significantly higher in D10 group than those in other groups (p < 0.0001, p < 0.0001, p = 0.002, p < 0.0001 and p < 0.0001, p = 0.046, p < 0.0001 and p = 0.002, respectively). Tissue MDA levels in D10 group were significantly higher than those in control, D5+Vit C and D10+Vit C groups (p = 0.028, p = 0.004, p = 0.031, respectively). SOD enzyme activity in D10 group was significantly lower than in control, D5+Vit C and D10+Vit C groups (p < 0.0001, p = 0.023 and p = 0.031, respectively). CONCLUSION: High dose dexmedetomidine can induce hepatic injury and oxidative stress in rats while pretreatment with vitamin C may be effective in protecting liver tissue against this newly recognized undesirable dexmedetomidine effect (Tab. 2, Fig. 5, Ref. 30). Text in PDF www.elis.sk.