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SUMMARY 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 explore the application of different doses of dexmedetomidine combined with general anesthesia in patients with traumatic tibiofibular fractures. Methods. A total of 120 patients with traumatic tibiofibular fractures treated in our hospital (January 2018–January 2021) were selected as the research subjects and equally grouped into group A, group B, group C, and group D according to the dosage of dexmedetomidine. Group B, group C, and group D were pumped with 0.3 μg/kg, 0.5 μg/kg, and 0.8 μg/kg load doses of dexmedetomidine before anesthesia induction, with the same doses for maintenance during surgery. Group A was intravenously pumped with the same amount of normal saline and received tracheal intubation after anesthesia induction, with propofol and remifentanil to maintain general anesthesia during surgery. Results. No notable differences in general data were observed among the groups (P > 0.05). Ramsay sedation scores of all groups showed a downward trend after drug withdrawal. At 10 min, 30 min, and 60 min, the scores of groups C and D were markedly higher than those of groups A and B (P P P > 0.05). The HRs at T1 and T2 in group C were slightly lower than those in group D (P > 0.05), and the HRs at T1 in groups A and B were remarkably higher than those in groups C and D, and were higher than those at T0 and T2 (P P P P > 0.05), the MAP levels in group A at T1 and T2 were obviously higher compared with groups C and D (P P P P P P

The report of bradycardia caused by propofol is increasing. In the experiment, we investigated the chronotropic function of propofol and the underlying mechanism. Rabbits of both sexes were randomly divided into 4 groups: propofol 5 mg/kg group, 10 mg/kg group, 15 mg/kg group, and sham group. Heart rate and frequency of vagal efferent discharge were recorded before the injection and 0, 0.5, 1, 2, and 10 min after the injection through intravenous mode. Then, their hearts were removed, and sinoatrial nodes were dissected. The action potentials of the sinus node pacemaker cells were recorded by the intracellular glass microelectrode technique, and the sinoatrial (SA) node was exposed to propofol 1, 3, 5, and 10 µM respectively. The action potentials were recorded after the sinoatrial nodes were exposed to each concentration of propofol for 15 min. Our results show that the heart rate significantly decreased, and the vagal efferent discharge was significantly increased at 0, 0.5, 1, and 2 min after the injection, respectively. Besides, as the dose increases, the magnitude of change shows a dose-dependent manner. Propofol exerts a negative chronotropic action on sinoatrial node pacemaker cells. The drug significantly decreased APA, VDD, RPF, and prolonged APD90 in a concentration-dependent manner. These effects may be the main mechanism of propofol-induced bradycardia in clinical study.