Dexmedetomidine protects against ischemia–reperfusion injury in rat skeletal muscle

• Published in: The Journal of surgical research 2014, Vol.186 (1), p.240-245
• Main Authors: Dong, Xu, MM, Xing, Qunzhi, MM, Li, Yu, MM, Han, Xuechang, MM, Sun, Lixia, MM
• Format: Article
• Language: English
• Subjects: Animals; Catalase - metabolism; Dexmedetomidine; Dexmedetomidine - therapeutic use; Glutathione - metabolism; Interleukin-1beta - blood; Ischemia–reperfusion injury; Malondialdehyde - analysis; Muscle, Skeletal - blood supply; Rats; Rats, Wistar; Reactive oxygen species; Reperfusion Injury - metabolism; Reperfusion Injury - prevention & control; Skeletal muscle; Surgery; Tumor Necrosis Factor-alpha - blood
• ISSN: 0022-4804; 1095-8673
• DOI: 10.1016/j.jss.2013.07.052

Abstract Background Dexmedetomidine (DEX) has been shown to decrease ischemia–reperfusion (I/R) injury in kidney and brain tissues. In this study, the effects of DEX were evaluated in skeletal muscle during I/R injury. Materials and methods Animals were divided into four groups: sham-operated (sham group), saline + I/R, DEX + I/R, and α-tocopherol + I/R groups. Hind limb ischemia was induced by clamping the common femoral artery and vein. After 4 h of ischemia, the clamp was removed and the animals underwent 2 h of reperfusion. Animals in the drug treatment group received DEX or α-tocopherol by intraperitoneal injection 1 h before reperfusion. We measured plasma concentrations of interleukin 1β and tumor necrosis factor α levels using an enzyme-linked immunosorbent assay. The right gastrocnemius muscle was harvested and immediately stored at −80°C for the assessment of superoxide dismutase (SOD) and catalase (CAT) activities as well as glutathione (GSH), malondialdehyde (MDA), and protein oxidation (PO) levels. DEX (25 μg/kg) and normal saline (10 mL/kg) were administered by intraperitoneal injection 1 h before reperfusion. Results Plasma tumor necrosis factor α or interleukin 1β levels increased significantly in the I/R group ( P