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Electro-acupuncture stimulation prevents remifentanil-induced postoperative hyperalgesia by suppressing spinal
1Department of Anesthesiology, Anhui Provincial Hospital Affiliated Anhui Medical University, Hefei, Anhui 230001, P.R. China.
Abstract:
The aim of the present study was to assess the effect of electro-acupuncture (EA) stimulation on remifentanil-induced postoperative hyperalgesia (RIPH) and the possible involvement of spinal microglia suppression. A model of RIPH was established using adult male Sprague-Dawley rats by administration of remifentanil at 0.08 mg/kg intravenously for 60 min. The Huantiao and Yanglingquan acupoints were stimulated continuously by EA (2 Hz, ~1 mA) for 90 min from before paw incision to the end of remifentanil administration. Sham acupoints were stimulated by EA in the sham group. Paw withdrawal threshold (PWT) and paw thermal withdrawal latency (PWL) were determined. Cluster of differentiation (CD)11b, tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 levels in spinal cord samples were measured using immunohistochemistry and ELISA. PWT and PWL values were decreased following the administration of remifentanill; however, following EA, PWT and PWL values increased compared with the sham group (P<0.05), indicating that EA alleviates remifentanil-induced RIPH. CD11b, TNF-α, IL-1β and IL-6 levels were increased following remifentanil administration and these effects were counteracted by EA (all P<0.05). In the sham group, no significant differences were observed in PWT and PWL values or CD11b, TNF-α, IL-1β and IL-6 levels compared with the control group, suggesting that EA was responsible for the reduction in CD11b and pro-inflammatory cytokine expression following remifentanil administration. The results of the present study demonstrated that EA at the Huantiao and Yanglingquan acupoints may reduce remifentanil-induced postoperative hyperalgesia, likely by inhibiting spinal microglia via reduction of CD11b and pro-inflammatory cytokine expression. However, these results are preliminary and require further validation.
Insights
Electro-acupuncture (EA) alleviates remifentanil-induced postoperative hyperalgesia by suppressing spinal microglia activation. This study shows EA reduces pain and inflammation markers, suggesting a potential therapeutic approach for managing postoperative pain.
Area of Science:
- Neuroscience
- Pain Management
- Pharmacology
Background:
- Remifentanil, an opioid analgesic, can paradoxically induce hyperalgesia (increased pain sensitivity) post-administration.
- Postoperative hyperalgesia poses a significant clinical challenge, necessitating novel therapeutic strategies.
- Spinal microglia activation is implicated in the development of opioid-induced hyperalgesia.
Purpose of the Study:
- To investigate the efficacy of electro-acupuncture (EA) in mitigating remifentanil-induced postoperative hyperalgesia (RIPH).
- To explore the potential role of spinal microglia suppression in EA's analgesic effects.
- To examine the impact of EA on pro-inflammatory cytokine expression in the spinal cord.
Main Methods:
- A rat model of RIPH was established using intravenous remifentanil administration.
- Electro-acupuncture was applied to the Huantiao and Yanglingquan acupoints.
- Pain behaviors (paw withdrawal threshold and latency) and spinal levels of CD11b, TNF-α, IL-1β, and IL-6 were assessed.
Main Results:
- EA significantly alleviated RIPH, as evidenced by increased paw withdrawal threshold and latency compared to the sham group.
- Remifentanil administration increased spinal CD11b and pro-inflammatory cytokine levels (TNF-α, IL-1β, IL-6).
- EA treatment counteracted these increases, reducing CD11b and cytokine expression.
Conclusions:
- Electro-acupuncture at specific acupoints effectively reduces remifentanil-induced postoperative hyperalgesia in rats.
- EA's mechanism likely involves the inhibition of spinal microglia activation and suppression of pro-inflammatory cytokine release.
- These findings suggest EA as a promising adjunct therapy for managing postoperative pain and hyperalgesia.
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