Hyperpolarizing Afterpotentials in C Fibers and Local Anesthetic Effects of Clonidine and Lidocaine

Abstract

Effects of clonidine and lidocaine on the hyperpolarizing after-potential (HAP) and frequency-dependent block in C fibers were examined on desheathed rabbit vagus nerves, using the sucrose gap technique. A single action potential (AP) was followed by a fast and a slow HAP. Clonidine, at concentrations from 0.05 to 50 µmol/l, decreased the fast HAP, while the AP amplitude was unchanged. At a 500 µmol/l concentration of clonidine, the fast HAP amplitude was similar to control, the slow HAP was increased, and the AP amplitude decreased. Lidocaine at 500 µmol/l delayed and broadened the HAP, making a distinction between fast and slow HAP impossible, and decreased and delayed the AP amplitude. In the presence of lidocaine (500 µmol/l), clonidine at concentrations from 0.05 to 500 µmol/l decreased the HAP amplitude, without modifying the lidocaine-induced shape of the HAP. The modifications of the HAP, however, do not contribute to the local anesthetic effects of clonidine, as the addition of clonidine (0.5 and 500 µmol/l) to Locke or lidocaine (500 µmol/l) solution does not enhance the frequency-dependent block (3 and 10 Hz) observed with either Locke or lidocaine solution alone.

Addition of clonidine or lignocaine to ropivacaine for supraclavicular brachial plexus block: a comparative study

“…(3,24) Although it is unlikely that the spinal and supraspinal effect is the mechanism that prolongs the analgesic effect of clonidine deposited at peripheral sites, analgesic agent, (25) suggesting that synergistic activity is more likely the mechanism for the prolonged analgesic duration observed with the use of clonidine. The direct action of clonidine, independent of its action on α2 receptor nerve fibre conduction, has been demonstrated in some studies, (16,26,27) indicating another possible mechanism for its action as a local anaesthetic additive. Hutschala et al have postulated that the effect of clonidine is local.…”

Intrathecal Clonidine Co-Administered With Hyperbaric Bupivacaine in Infra-Umbilical Surgery - A Dose Response Study

“…The receptors are located on primary afferent terminals (both at peripheral and spinal endings), on neurons in the superficial laminae of the spinal cord, and within several brainstem nuclei implicated in analgesia, supporting the possibility of analgesic action at peripheral, spinal, and brainstem sites. [17] Clonidine does produce a minor degree of nerve conduction blockade at high concentrations, however, with some preference for C-fibers, [18] Section: Anaesthesia which are important neuronal structure for pain transmission. Some experimental data suggest that intrathecal injection of clonidine increases cerebrospinal fluid acetylcholine concentrations [19] and intrathecal injection of cholinesterase inhibitors enhances analgesia.…”

Dosis-Wirkungsbeziehung von Clonidin zu epidural appliziertem Ropivacain bei orthopädischen Eingriffen der unteren Extremität

“…Clonidin wird auch ein lokaler, direkt am Nerven angreifender Effekt zugesprochen [26]. Dabei wird nach Gaumann et al [9] durch Clonidin ein Verstärkungseffekt auf die lidocainevozierte Inhibition des C-FaserAktionspotentials gesehen. Starke et al [27] stellten auf der Cornea des Hasen fest, daß Clonidin 140mal potenter wirkte als Procain.…”