Issn Print: 0265-0215

Publication Date: 2006/06/01


Print

Role of spinal Substance P in expression of acute opioid hyperalgesia under normal and neuropathic conditions: A-926

M. A. Docquier; V. Collet; M. De Kock; P. Lavand'homme

    loading  Checking for direct PDF access through Ovid

Excerpt

Background: We previously reported acute opioid hyperalgesia (OH) supported by increased MACbar under Sevoflurane anesthesia (MACbar SEVO) and very low dose of IV Sufentanil (SUF).(1) While μ-agonists inhibit noxious stimulus-evoked Substance P (SP) (NK1-Receptor ligand) release, sustained morphine treatment and nerve injury increase both spinal sensitivity to SP and NK1-R expression. (2,3) The study evaluates the role spinal SP in acute OH development in normal (C) and neuropathic (NP) rats.
Materials and Methods: In adult male Wistar rats (n = 5 per group), the MACbar SEVO was determined by tail clamp stimulus before and during low dose SUF infusion (0.005μg/kg/h) in C and NP rats (3 months after partial ligation of sciatic nerve). Intrathecal (IT) saline or NK1-R antagonist 500μg (L-732,138) was administered before MACbar SEVO determinations. Results are expressed as MACbar SEVO (%, mean ± SD) and % rats developing acute OH defined as >20% increase of MACbar SEVO after SUF infusion. Statistics used ANOVA and Χ2 tests.
Results:
Conclusion: In contrast with normal rats, NP rats do not display acute OH. Spinal plasticity already triggered pain facilitatory processes masking OH. Pretreatment with IT NK1-R antagonist prevents acute OH in normal rats but restores its development in NP rats. Neuroadaptive changes in spinal regulatory mechanisms might be involved.
    loading  Loading Related Articles