Background Several studies have shown that dexmedetomidine (DXM), a selective α2-adrenoceptor agonist, also has neuroprotective effects. However, its effect on impaired peripheral nerve regeneration has not been studied. Materials and Methods Forty-five Sprague-Dawley rats were randomly assigned to three groups: group 1 (control SHAM), group 2 (sciatic nerve injury + normal saline), and group 3 (sciatic nerve injury + DXM). The rats of group 3 were subdivided into the following three groups: DXM 0.5, 6, and 20 μg·kg−1 (groups 3A, 3B, and 3C, resp.). The sciatic nerve injury was assessed for nerve regeneration at 2 and 6 weeks. Results There were no differences between groups 2 and 3 in their sciatic functional index (SFI) values or histological findings at 2 weeks postinjury. However, SFI differences were statistically significant at 6 weeks postinjury in group 3. The gross findings with H&E staining showed that the number of axons was higher in group 3 than in group 2. There was no histological difference according to the DXM concentration. Conclusion The coincidental functional and histological assessment results of this study suggest that DXM for 6 weeks positively affects damaged peripheral nerves.

Dexmedetomidine (DMT) is a selective a-2 agonist that has both sedative and analgesic effects [1][2][3]. It is clinically widely used because it induces mild respiratory depression in patients who are responsive to mild tactile stimulation during sedation [4][5][6]. Therefore, DMT is an effective sedative to reduce anxiety in patients undergoing regional anesthesia.The recommended dose of DMT includes a loading dose of 1 mg/kg over 10 minutes, followed by a continuous infusion of 0.2-0.7 mg/kg/h [7]. In addition to its sedative properties, DMT can also reduce heart rate (HR), cardiac output, and circulating catecholamine in a dose-dependent fashion.