Clonidine Has Comparable Effects on Spontaneous Sympathetic Activity and Afferent Aδ– and C-Fiber-mediated Somatosympathetic Reflexes in Dogs

Abstract

Clonidine, an alpha 2-adrenergic agonist, has been studied as an adjunct or alternative to spinal opioids in the management of moderate to severe pain. This study examined the relative effects of clonidine on efferent spontaneous sympathetic activity and afferent A delta and C fiber-mediated somatosympathetic responses. Spontaneous and evoked sympathetic activity in renal sympathetic nerves, mediated by A delta and C fibers by means of supramaximal electrical stimulation of the radial and tibial nerves, were observed in anesthetized dogs. Incremental doses of clonidine were administered intrathecally or intravenously in each of five preparations followed by intravenous naloxone 2 mg and yohimbine 5 mg. Both spontaneous sympathetic outflow and afferent A delta- and C fiber-mediated somatosympathetic responses evoked by tibial nerve stimulation were depressed in a similar dose dependent manner by clonidine administered intrathecally or intravenously in a dose ratio of approximately 1:4. Intrathecal clonidine inhibited and eliminated both local spontaneous sympathetic outflow and tibial nerve evoked sympathetic responses but had no significant depressant effect on the radial nerve evoked sympathetic reflexes. When administered intravenously clonidine had a similar depressant effect on both radial and tibial nerve elicited reflexes and spontaneous sympathetic activity. Clonidine, administered intrathecally or intravenously, has a similar depressant effect on both spontaneous sympathetic outflow and afferent A delta- and C fiber-mediated somatosympathetic reflexes. When administered intrathecally it has little effect on reflexes evoked via the descending pathway by radial nerve stimulation.