DEPRESSION OF NOCICEPTIVE SYMPATHETIC REFLEXES BY THE INTRATHECAL ADMINISTRATION OF MIDAZOLAM

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Abstract
The effect of the intrathecal administration of midazolam 0.5–1.0 mg in 1–2 ml of physiological saline solution, has been observed on responses evoked in renal sympathetic nerves by supramaximal electrical stimulation of radial and tibial nerves. In artificially ventilated dogs anaesthetized with a-chloralose, the intrathecal administration of midazolam caused a marked depression of reflexes evoked from the tibial nerve but had no effect on either spontaneous sympathetic activity or reflexes evoked by radial nerve stimulation. Neither the small amount (1–2 ulitre) of benzyl alcohol, present as a preservative (administered intrathecally), nor midazolam 1 mg kg−1 i.v. caused any significant depression of the evoked somato-sympathetic reflexes. The effects of intrathecal midazolam were reversed by the benzodiazepine antagonists Ro 15–1788 1 mg kg−1 i.v. and Ro 15–3505 1–2 mg kg−1 i.v. but not by naloxone 2 mg i.v. It is suggested that the antinociceptive effect of locally applied midazolam could be the result of a non-opioid GABA-mediated system which may have implications in the management of pain.