Dexmedetomidine (Dex) is a novel Alpha 2-adrenoceptor agonist. It decreases sympathetic tone and
attenuates the stress responses to anesthesia and surgery. People exposed to cold suffer unpleasant
thermal pain, which is experienced as stress and causes the release of noradrenaline from the sympathetic terminals. The present study investigated the effects of cold stress and dexmedetomidine on
chronic constriction injury (CCI) model of the sciatic nerve in rats. Sixty four male Wistar rats were
divided into seven groups of eight rats each: repeated cold stress (RCS) group, sham RCS group, CCI
group, sham CCI group, Dex-treated group received a single dose of Dex (5 μg/kg), CCIþDex group,
CCIþRCS group. Interleukin-6 (IL-6) and tumor necrosis factor- alpha (TNF-α) levels in the serum were
measured by enzyme-linked immunosorbent assay. The mean body weight of CCI, RCS, CCIþRCS,
CCIþDex and RCSþDex groups decreased significantly compared with pre-values. Dexmedetomidine
and CCI caused significant changes of the systolic, diastolic and mean blood pressure. Both RCS and CCI
groups showed significant decreased of reaction time in the hot plate test. The RCS and CCI groups
demonstrated a significant mechanical hyperalgesia, while pain threshold was increased in the RCSþDex
group. A significant decrease of serum IL-6 and TNF-α was demonstrated in CCIþRCS and CCIþDex
groups. The therapeutic effectiveness of dexmedetomidine in neuropathic pain may be through inhibition of proinflammatory cytokines, primarily IL-6 and TNF-α. Moreover, cold stress may result in increased resistance to neuropathic pain.