title: Dexmedetomidine protects against ischemia-reperfusion injury in rat skeletal muscle.
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.
  
  
  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 < 0.01 compared with sham group) and decreased significantly in the DEX group (P < 0.01 compared with I/R group). Muscle tissues of the I/R group had significantly decreased SOD, GSH, and CAT activities and increased levels of MDA and PO content compared with the sham group. The activity of antioxidant enzymes in the DEX + I/R group was greatly elevated compared with that in the I/R group (SOD, 1.068 ± 0.120 versus 0.576 ± 0.072 U/mg protein; GSH, 2.436 ± 0.144 versus 1.128 ± 0.132 μmol/g; and CAT, 69.240 ± 6.456 versus 31.884 ± 6.312 U/mg protein; P < 0.01), whereas the levels of MDA and PO content were clearly reduced (23.268 ± 3.708 versus 53.604 ± 5.972 nmol/g protein and 1.908 ± 0.192 versus 5.208 ± 0.612 nmol/mg protein, respectively; P < 0.01). Moreover, DEX exhibited more potent antioxidant activity than vitamin E in the skeletal muscle I/R.
  
  
  CONCLUSIONS
  We found that DEX exhibits protective effects against skeletal muscle I/R injury. These results underscore the necessity of human studies with DEX to determine if it is beneficial for preventing skeletal muscle I/R injury.
authors.affiliation: Department of Anesthesiology, The First Affiliated Hospital, Henan Science and Technology University, Luoyang, Henan, China.
authors.forename: Xu
authors.initials: X
authors.lastname: Dong
authors.forename: Qunzhi
authors.initials: Q
authors.lastname: Xing
authors.forename: Yu
authors.initials: Y
authors.lastname: Li
authors.forename: Xuechang
authors.initials: X
authors.lastname: Han
authors.forename: Lixia
authors.initials: L
authors.lastname: Sun
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D020927:Dexmedetomidine / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D053583:Interleukin-1beta / Q000097:blood; D008315:Malondialdehyde / Q000032:analysis; D018482:Muscle, Skeletal / Q000098:blood supply*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D020927:Dexmedetomidine; D002374:Catalase; D005978:Glutathione
keywords: Dexmedetomidine; Ischemia–reperfusion injury; Reactive oxygen species; Skeletal muscle