• J W Leem, Y Choi, S M Han, M J Yoon, J Y Sim, and S W Leem.
• Department of Anesthesiology, University of Ulsan College of Medicine, 388-1 Poongnap-dong, Songpa-gu, Seoul, Korea.
• Reg Anesth Pain Med. 2000 Nov 1;25(6):620-5.

Background And ObjectivesClonidine, an alpha(2)-adrenergic agonist, has been shown to prolong local anesthesia. It appears that clonidine by itself produces conduction block by acting on peripheral nerves. However, whether clonidine-induced conduction block is mediated through alpha(2)-adrenergic receptors remains unclear. The purpose of this study was to see if clonidine's nerve-blocking action was through alpha(2)-adrenergic receptors by examining clonidine's action in the presence of alpha(2)-adrenergic antagonists.MethodsThe compound action potentials (CAPs) evoked by electrical stimuli were recorded from the isolated rat sciatic nerve in a recording chamber. Conduction block was examined by analyzing CAPs with regard to peak amplitude and time-to-peak in the presence of clonidine alone or clonidine plus alpha(2)-adrenergic antagonist yohimbine or idazoxan.ResultsBoth clonidine and yohimbine produced concentration-dependent, reversible, conduction block. Based on concentration-response relationships, the 50% of effective concentration (EC(50)) were estimated to be 1.61 +/- 0.51 mmol/L (mean +/- SD) for clonidine and 51.4 +/- 27.2 micromol/L for yohimbine. A mixture of equal volumes of 2.07 mmol/L clonidine and 55.6 micromol/L yohimbine produced conduction block to a level close to the mean value between conduction blocks induced by 2.07 mmol/L clonidine alone and 55.6 micromol/L yohimbine alone. Addition of idazoxan, a more specific alpha(2)-adrenergic antagonist than yohimbine, to clonidine was without effect on clonidine-induced conduction block.ConclusionsThe results indicated that the mixture of clonidine and yohimbine, in which either drug inhibited impulse conduction, produced conduction block in an additive manner, and that clonidine-induced conduction block was not reversed by coapplication with a specific alpha(2)-adrenergic antagonist idazoxan. These data suggest that clonidine's effects likely depend on mechanisms not mediated by alpha(2)-adrenergic receptors.

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