• Adnan Tüfek, Savaş Kaya, Orhan Tokgöz, Uğur Firat, Osman Evliyaoğlu, Feyzi Çelik, and Haktan Karaman.
• Department of Anesthesiology, School of Medicine, Dicle University, 21280 Diyarbakır, Turkey. adnantufek@hotmail.com
• Clin Invest Med. 2013 Jan 1;36(2):E95-102.

PurposeThis study was designed to assess the correlation between the neuroprotective effect of dexmedetomidine and oxidative stress, neural inflammation and mast cell stability in rats with bupivacaine-induced sciatic nerve toxicity.MethodsForty adult Wistar Albino rats, eight rats per group, were used. Saline (0.3 ml of 0.9%), dexmedetomidine (20 µg/kg), 0.5% bupivacaine or 0.5% bupivacaine+dexmedetomidine (20 µg/kg) was injected into the sciatic nerve. A control group of rats received no injection. Fourteen days after injection, the sciatic nerves were harvested and total oxidant status, total anti-oxidant status, paraoxonase-1, galectin-3 and matrix metalloproteinase 2 and 9 levels were measured in the sciatic nerves. In addition, the presence and status of inflammation, edema, and mast cells were evaluated histopathologically.ResultsThe combination of dexmedetomidine and bupivacaine alleviated oxidative stress. In addition, it decreased matrix metalloproteinase 9 and galectin-3 levels and increased matrix metalloproteinase 2 levels. Moreover, it stabilized recruited mast cells at the injury site; however, it did not significantly decrease inflammation or edema.ConclusionDexmedetomidine may ameliorate bupivacaine-induced neurotoxicity by modulating mast cell degranulation. The neuroprotective effect of dexmedetomidine may make it a suitable adjuvant agent to local anesthetics in peripheral nerve blocks.

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