Dexmedetomidine, α2-adrenoceptor agonist, does not induce apoptosis in the brachial plexus of rats

Abstract

Dexmedetomidine (Precedex) is a selective α2-adrenoceptor agonist that shows opioid-sparing effects with reduced inhalational anesthetic requirement. Since the possibility that dexmedetomidine could induce nerve degeneration has not been completely ruled out, we evaluated whether it can induce apoptosis in rats when used in a nerve block. We performed hematoxylin and eosin staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays, immunohistochemistry for caspase-3 and neurofilament, and western blotting for BAX, Bcl-2, and nerve growth factor (NGF) in the brachial plexus of rats. The axillary brachial plexus was carefully exposed and 100 μl (40 µg/kg) dexmedetomidine was administered directly. Rats were sacrificed at 6 h, 12 h, or 24 h after dexmedetomidine administration. In the present study, dexmedetomidine did not exert any effects on histological findings and neurofilament expression. The number of TUNEL-positive and caspase-3-positive cells in the brachial plexus did not change following dexmedetomidine administration. The Bcl-2 to BAX ratio temporarily increased and then returned to the control level at 24 h after dexmedetomidine administration. Expression of NGF in the brachial plexus temporarily increased and then returned to the control level 12 h after dexmedetomidine administration. The results of our study demonstrated that dexmedetomidine did not induce apoptosis and degeneration when used in the brachial plexus.