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Vol. 282, Issue 1, 86-92, 1997
The Department of Anesthesia, Bowman Gray School of Medicine of
Wake Forest University, Winston-Salem, North Carolina
Intravenous opioids cause analgesia and increase release of ACh in
spinal cord dorsal horn in animals, and these effects are enhanced by
intrathecal neostigmine injection. The purpose of the current study was
to test whether intrathecal neostigmine enhanced analgesia and
increased cerebrospinal fluid concentrations of ACh over those induced
by i.v. alfentanil in volunteers, and also to test whether neostigmine
enhanced alfentanil-induced side effects. After human studies committee
approval, 40 healthy volunteers received an intrathecal injection of
saline or neostigmine (50, 100 or 200 µg) followed in 60 min by a
computer-controlled, stepped i.v. infusion of alfentanil to escalating
targeted plasma concentrations. Pain report to hand and foot immersion
in ice water, sedation, nausea, weakness, vital signs, end-tidal
CO2 and oxyhemoglobin saturation were measured 60 min after
spinal injection and at the end of each 20-min alfentanil infusion.
Cerebrospinal fluid was sampled once after drug administration.
Intrathecal neostigmine alone caused analgesia in the foot but not in
the hand, and was accompanied by leg weakness, whereas IV alfentanil
alone caused equivalent analgesia in both the hand and the foot and was
accompanied by nausea, sedation, increased end-tidal CO2
and decreased oxyhemoglobin saturation. Neostigmine enhanced analgesia
but not respiratory effects induced by i.v. alfentanil; it also
enhanced nausea and sedation. Intravenous alfentanil increased
cerebrospinal fluid ACh concentration, and neostigmine enhanced this
change. These data in humans are consistent with a spinal cholinergic
mechanism of i.v. opioid analgesia. Because neostigmine enhances both
analgesia and side effects induced by i.v. alfentanil, the clinical
utility of their use in combination will depend on the relative
strength of these interactions.
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