Low-dose lidocaine suppresses experimentally induced hyperalgesia in humans

Citation
W. Koppert et al., Low-dose lidocaine suppresses experimentally induced hyperalgesia in humans, ANESTHESIOL, 89(6), 1998, pp. 1345-1353
Citations number
38
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ANESTHESIOLOGY
ISSN journal
00033022 → ACNP
Volume
89
Issue
6
Year of publication
1998
Pages
1345 - 1353
Database
ISI
SICI code
0003-3022(199812)89:6<1345:LLSEIH>2.0.ZU;2-V
Abstract
Background: The antinociceptive effects of systemically administered local anesthetics have been shown in various conditions, such as neuralgia, polyn europathy, fibromyalgia, and postoperative pain. The objective of the study was to identify the peripheral mechanisms of action of low-dose local anes thetics in a model of experimental pain. Methods: In a first experimental trial, participants (n = 12) received lido caine systemically (a bolus injection of 2 mg/kg in 10 min followed by an i ntravenous infusion of 2 mg kg(-1).h(-1) for another 50 min). In a second t rial, modified intravenous regional anesthesia was administered to exclude possible central analgesic effects. In one arm, patients received an infusi on of 40 mi lidocaine, 0.05%; in their other arm, 40 mi NaCl, 0.9%, served as a control. In both trials, calibrated tonic and phasic mechanical and ch emical (histamine) stimuli were applied to determine differentially the imp airment of tactile and nociceptive perception. Results; Mechanical sensitivity to touch, phasic mechanical stimuli of noxi ous intensity, and heat pain thresholds remained unchanged after systemic a nd regional application of the anesthetic. In contrast, histamine-induced i tch (intravenous regional anesthesia), axon reflex flare (systemic treatmen t), and development of acute mechanical hyperalgesia during tonic pressure (12 N; 2 min) of an interdigital web was significantly suppressed after bot h treatments, Conclusions: Increasing painfulness during sustained pinching has been attr ibuted to excitation and simultaneous sensitization of particular A delta- and C-nociceptors. This hyperalgesic mechanism seems to be particularly sen sitive to low concentrations of lidocaine. These findings confirm clinical experience with lidocaine in pain states dominated by hyperalgesia.