OBJECTIVE:The aim of this study was to investigate whether dexmedetomidine could reduce tourniquet-induced skeletal muscle injury. METHODS: C57BL6 male mice were randomly assigned to sham, ischemia/reperfusion, and dexmedetomidine groups. Mice in the ischemia/ reperfusion and dexmedetomidine groups received normal saline solution and dexmedetomidine intraperitoneally, respectively. The sham group underwent the same procedure as the ischemia/reperfusion group, with the exception of tourniquet application. Subsequently, the ultrastructure of the gastrocnemius muscle was observed, and its contractile force was examined. In addition, Toll-like receptor 4 and nuclear factor-κB expression within muscles was detected by Western blot. RESULTS: Dexmedetomidine alleviated myocyte damage and increased the contractility of skeletal muscles. Moreover, dexmedetomidine significantly inhibited the expression of Toll-like receptor 4/nuclear factor-κB in the gastrocnemius muscle. CONCLUSION: Taken together, these results demonstrate that dexmedetomidine administration attenuated tourniquet-induced structural and functional impairment of the skeletal muscle, partly through inactivation of the Toll-like receptor 4/nuclear factor-κB pathway.

Objective To investigate whether dexmedetomidine (Dex) can reduce the severity of tourniquet-induced lung injury. Methods 36 patients undergoing total knee arthroplasty with a tourniquet were randomly assigned to the control (ischemia/reperfusion [I/R]) group and Dex group. Patients in the Dex group received a loading dose of Dex (0.8 μg/kg over 10 min intravenously) followed by continuous infusion of Dex (0.5 μg/kg/h intravenously) until the end of the surgery. The I/R group received an equal amount of 0.9% saline instead of Dex. The serum concentrations of tumor necrosis factor-α (TNF-α), Clara cell protein (CC-16), soluble receptor for advanced glycation end products (sRAGE), and brain-derived neurotrophic factor (BDNF) were measured and arterial blood gas analysis was performed before anesthesia and 30 min, 6 h, and 24 h after tourniquet release. Results In the I/R group, compared with baseline, the TNF-α, CC-16, and sRAGE concentrations were higher ( p < 0.05) and the BDNF concentration was lower ( p < 0.05) at most time points. In the Dex group, the TNF-α, CC-16, and sRAGE concentrations were lower than those in the I/R group ( p < 0.05), whereas the concentration of BDNF was higher ( p < 0.05). In the arterial blood gas analysis, the Dex group showed a significantly higher partial pressure of oxygen and arterial/alveolar oxygen tension ratio ( p < 0.05) and a significantly lower alveolar/arterial oxygen tension difference than the I/R group ( p < 0.05). Conclusion Dex administration partly inhibits the release of proinflammatory cytokines, affording protection against tourniquet-induced lung injury.