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*Department of Anesthesiology and Pain Medicine, University of California, Davis,
Section of Neurobiology, Physiology and Behavior, University of California, Davis,
Department of Anesthesiology, Ehime University, Matsuyama, Japan
Address correspondence and reprint requests to Joseph F. Antognini, MD, Department of Anesthesiology TB-170, University of California, Davis, Davis, CA 95616. Address e-mail to jfantognini{at}ucdavis.edu.
Etomidate is a widely used IV anesthetic, but little is known about its analgesic properties, in particular, its effects on spinal cord neuronal responses to noxious stimuli. We hypothesized that etomidate would depress lumbar neuronal responses to noxious heat. Rats (n = 15) were anesthetized with isoflurane (1.2%) and laminectomy was performed to record single unit activity. Lumbar neuronal responses to noxious thermal (52°C, 12 s) stimulation of the hindpaw were recorded before and every 2 min (up to 13 min postinjection) after administration of etomidate. The responses at peak effect of etomidate (as a percentage of the control response) were 63% ± 16%, 63% ± 16%, 38% ± 25%, 36% ± 30%, and 41% ± 26% for the 0.125, 0.25, 0.5, 1 and 2 mg/kg doses, respectively. The responses quickly recovered, usually by the 10-min period postinjection. Similar responses were obtained in decerebrate, isoflurane-free rats administered etomidate and in isoflurane-anesthetized rats administered propofol. These data demonstrate that etomidate depresses spinal cord neuronal responses to noxious stimulation and is a possible mechanism by which this drug might produce analgesia.
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