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Vol. 280, Issue 2, 876-883, 1997
W. M. Keck Foundation Center for Integrative Neuroscience and
Departments of Anatomy and Physiology, University of California San
Francisco, San Francisco, California
Injection of dilute formalin into the hindpaw produces brief (phase 1)
and persistent (phase 2) nociceptive responses in the rat. We recently
reported that ongoing peripheral nerve input is required for the
expression of behavioral and cardiovascular responses during phase 2. Here we evaluated the contribution of central and peripheral
sensitization mechanisms, generated during phase 1, to the magnitude
and temporal profile of phase 2. During phase 1, we administered
analgesic doses of an ultrashort-acting opioid, remifentanil (i.v.
administration from 0-5 min after 5.0% formalin injection), or
anesthetic concentrations of halothane (2.1%). Inhibition of phase 1 did not reduce the magnitude of flinching and cardiovascular responses
during phase 2, but it did delay their onset and/or termination. Longer
remifentanil infusions (0-15 or 0-30 min) produced even longer delays
(up to 30 min) in the onset and termination of flinching during phase 2; however, when remifentanil was administered during the early part of
phase 2 (15-30 or 15-45 min), it did not prolong the time to
termination of phase 2. Continuous infusion (10 mg/kg/hr i.v.) of a
peripherally acting opiate antagonist, naloxone methiodide, did not
reduce the antinociception produced by remifentanil during phase 1 but
almost completely reversed the delay in the onset and termination of
phase 2. We conclude that central sensitization mechanisms during phase
1 do not influence the magnitude of phase 2. We also hypothesize that
remifentanil interacts with peripheral opioid receptors to impede the
formalin-evoked synthesis and/or release of proinflammatory compounds
during phase 1 and thus delay phase 2.
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