Öz İnhalasyon anesteziklerinin oksidatif stres ve serbest radikallerin oluşumunda etkili olduğu bilinmektedir. Bu çalışmanın amacı, desfluranın bu etkilerini araştırmak ve farklı akımlarda oluşan değişiklikleri saptamaktır. Fareler üç gruba ayrıldı (10 fare / grup). Birinci grup kontrol grubu idi. İkinci grupta, ketamin ile sedasyon sağlanan farelere bir cam kutuda % 100 oksijen içerisinde % 6 konsantrasyonda, 20 dakika boyunca, 8 lt / dk akış hızında desfluran verildi. Üçüncü grupta bir cam

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... u içerisinde ketamin ile sedasyon sağlanmış farelere, % 100 oksijen içerisinde % 6 konsantrasyonda, 20 dakika boyunca, 2 lt / dk akış hızında desfluran verildi. Biyokimyasal parametreler ölçüldü. Serum, beyin, karaciğer dokusu MDA ve SOD düzeyleri yüksek akım grubunda kontrol ve düşük akım grubundan anlamlı olarak daha yüksek bulundu. Her iki gruba göre serum GPx düzeyleri yüksek akım grubunda anlamlı olarak düşüktü. Serum, karaciğer ve beyin dokusunda ADMA düzeyleri yüksek akım grubunda anlamlı olarak yüksek bulundu. Her üç grup arasında serum 8-OHdG seviyelerinde anlamlı fark yoktu. Beyin ve karaciğer dokusu 8-OHDG düzeyleri her iki grupta kontrol grubuna göre daha yüksekti. Desfluran anestezi modelinde, desfluranın aynı konsantrasyonlarda düşük akımda kullanıldığında oksidatif stresi azalttığı, yüksek akımda kullanıldığında ise oksidatif stresi arttırdığı görülmüştür. Abstract It is known that inhalation anesthetics are effective in the formation of oxidative stress and free radicals. The purpose of this study is to investigate these effects of desflurane and to detect changes in different flows. The rats were divided into three groups (10 mice/group). The first group was the control group. In the second group, mice were sedated with ketamine and given desflurane at a concentration of 6% in a 100% oxygen flow at a flow rate of 8 lt / min in a glass box for 20 minutes. The third group was comprised of ketamine-sedated mice that were given desflurane at a concentration of 6% in a 100% oxygen flow at a flow rate of 2 lt/min in a glass box for 20 minutes. Biochemical parameters were measured using commercial kits. Serum, brain, liver tissue MDA and SOD levels were significantly higher in the high flow group than in the control and low flow group. Serum GPx levels were significantly lower in the high flow group compared to both groups. ADMA levels in the serum, liver, and brain tissue were significantly higher in the high flow group. There was no significant difference in serum 8-OHdG levels between all three groups. Brain and liver tissue 8-OHDG levels were higher in both groups than control group. It has been observed that the use of low flow fresh gas even in the same concentrations of desflurane anesthesia models decreases oxidative stress whereas the use of high flow increases oxidative stress. All the animals were fasted for 16 hrs, but still allowed free access to drinking tap water, before the commencement of our experiments C57BL/6, 6-8 week old female mice were randomly divided into 3 equal groups, each containing 10 mice.Group 1 (control group): Received ketamine for sedation. Group 2 (low flow): Received ketamine for sedation. Later, desflurane was inhalated for anesthesia at a concentration of 6% in a 100% oxygen flow at a flow rate of 2 lt / min for 20 minutes. Group 3 (high flow): Received ketamine for sedation. Later, desflurane was inhalated for anesthesia at a concentration of 6% in a 100% oxygen flow at a flow rate of 8 lt / min for 20 minutes. At the end (20 minutes) of anesthesia period, animals were sacrificed. Blood and tissue samples were removed, tissues were washed in ice-cold PBS and weighed. Serum and tissue preparation At the end of this study, samples of blood, liver and brain tissues of each mouse were taken. The mouse tissues were weighed and 2. Zhang W, Liu M, Zang Z, et al. Effect of different anesthesia methods on erythrocyte immune function in mice. Asian Pac J Trop Med. 2013;6(12):995-998. 3. Türkan H, Aydın A, Sayal A, et al. The effect of sevoflurane and desflurane on markers of oxidative status in erythrocyte. Toxicol Ind Health. 2011; 27(2):181-186. 4. Schilling T, Kozlan A, Kretzschmar M, et al.