An Analgesic Mechanism of Intravenous Lidocaine Hydrochloride : Suppression of Dorsal-horn Nociceptive Neurons

To elucidate the mechanisms of analgesic action of intraveously administered local anesthetics, effects of lidocaine hydrochloride on dorsal-horn nociceptive neurons were studied in spinal cord transected, decerebratecl cats utilizing extracellular microelectrode recording techniques. All single units studied (n=37) responded to high threshold mechanical as well as noxious heat stimuli (radiant heat : using Hardy-Wollf-Goodell Dolorimeter). The mean spontaneous discharge frequency of the neurons studied was 9.5 ± 1.0 (mean ± 1. S.E.) I.P.S. (impulse per second). When radient heat stimuli (skin temp. 49 ℃) were given, the mean value of the average discharge frequency increased to 33.9 ± 2.5 I.P.S.. Lidocaine 2.5, 5.0, and 10.0 mg/kg i. v. produced dose related suppression of both spontaneous activities and responses to noxious heat stimulation. By above doses of lidocaine, the maximum suppression of the pontaneous activities observed at 3 to 7 min after lidocaine i. v. were 37, 68 and 75 percent, respectively; those of heat evoked response were 17, 48 and 61 percent, respectively (p<0.05). The threshold skin temperature to noxious heat stimuli increased from 44.7 ± 0.4 ℃ (during control) to 46.3 ± 0.7 ℃ with lidocaine 5.0 mg/kg (p<0.05), to 47.8 ± 0,8 ℃ with lidocaine 10.0 mg/kg (p