• N Liu, F Bonnet, L Delaunay, N Kermarec, and G D'Honneur.
• Département d'Anesthésie Réanimation, Hôpital Henri Mondor, Créteil, France.
• Br J Anaesth. 1993 May 1;70(5):515-8.

AbstractExtradural clonidine produces analgesia, with sedation, hypotension and bradycardia, in postoperative patients. This study assessed if oral yohimbine would reverse these side effects. We studied 30 ASA I-II patients undergoing orthopaedic surgery. After operation they were allocated randomly to three groups to receive placebo, extradural clonidine 450 micrograms or extradural clonidine 450 micrograms plus oral yohimbine 16 mg. Pain score was measured on a visual analogue scale (VAS); sedation was assessed on a simple scale graded from 0 (awake and alert) to 3 (deeply sedated, awakening after tactile stimulations) and heart rate and arterial pressure were monitored for 5 h. Yohimbine reversed the sedation induced by extradural clonidine, but also shortened the duration of analgesia (31 (SD 15) min, 186 (72) min and 126 (52) min in the placebo, extradural clonidine and extradural clonidine+yohimbine groups, respectively) (P < 0.05), and did not reduce the hypotension and bradycardia related to clonidine administration. These results suggest that alpha 2 adrenoceptors are mediators of the sedation induced by clonidine and that the haemodynamic effects are not related to stimulation of supraspinal alpha 2 receptors.

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