After Dexmedetodine administration we expected bradycardia due to a decrease in noradrenalinerelease, a decrease in centrally mediated sympathetic tone, and an increase in vagal activity.

However, as observed by Arain et al, Al-Mustafaet all. and Mahmoud et all., Dexmedetomidine could have rebound effect with the postsynaptic vascular smooth muscle to cause vasoconstriction and it is possible that the sympathoinhibitory effects of Dexmedetomidine were slightly opposed by direct α-2 mediated vasoconstriction.