Articles: hyperalgesia.
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Neuroscience letters · Oct 2009
Acute and chronic fentanyl administration causes hyperalgesia independently of opioid receptor activity in mice.
Although mu-receptor opioids are clinically important analgesics, they can also paradoxically cause hyperalgesia independently of opioid receptor activity, presumably via the action of neuroexcitatory glucoronide metabolites. However, it is unknown whether the commonly used mu-receptor opioid analgesic fentanyl, which is not subject to glucuronidation, can also induce hyperalgesia independently of opioid receptor activity. Thus, here we examined whether fentanyl increases nociception on the tail-withdrawal test in CD-1 mice concurrently treated with the opioid receptor antagonist naltrexone or in opioid receptor triple knock-out mice lacking mu, delta, and kappa opioid receptors. ⋯ MK-801 blocked and reversed hyperalgesia caused by the acute injection and continuous infusion of fentanyl, respectively, in naltrexone-treated CD-1 mice, indicating the contribution of NMDA receptors to fentanyl hyperalgesia. These data show that the synthetic opioid fentanyl causes hyperalgesia independently of prior or concurrent opioid receptor activity or analgesia. Since the biotransformation of fentanyl does not yield any known pronociceptive metabolites, these data challenge assumptions regarding the role of neuroexcitatory metabolites in opioid-induced hyperalgesia.
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Randomized Controlled Trial
[The effects of lornoxicam in preventing remifentanil-induced postoperative hyperalgesia].
Intraoperative remifentanil administration results in acute opioid tolerance that is manifested by increased postoperative pain, opioid requirement and specifically peri-incisional hyperalgesia. The aim of this study was to investigate the effect of lornoxicam in preventing remifentanil-induced hyperalgesia. ⋯ Lornoxicam administered preemptively prevented remifentanil-induced hyperalgesia.
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J Neurosurg Anesthesiol · Oct 2009
Systemic lidocaine inhibits remifentanil-induced hyperalgesia via the inhibition of cPKCgamma membrane translocation in spinal dorsal horn of rats.
Remifentanil is being used increasingly as one component of total intravenous anesthesia. Severe postoperative pain has occasionally been reported with discontinuation of remifentanil. This study was designed to determine the involvement of conventional protein kinase Cgamma (cPKCgamma) in the inhibitory action of lidocaine on remifentanil-induced hyperalgesia of rats after propofol-remifentanil-based anesthesia. ⋯ After plantar incision, the withdrawal threshold on both the contralateral and the ipsilaeral side at 30, 120, and 300 minutes postanesthesia in group R was significantly lower than in groups P, RL, and L (P<0.05). Both immunoblotting and immunofluorescence showed that cPKCgamma membrane translocation increased in dorsal horn neurons of propofol-remifentanil-based anesthetized rats, which could be inhibited by systemic lidocaine. These results suggested that increased cPKCgamma membrane translocation was involved in remifentanil-induced hyperalgesia, which was inhibited by systemic lidocaine and may contribute to reduced postoperative pain in rats after propofol-remifentanil-based anesthesia.
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Anesthesia and analgesia · Oct 2009
Activation of extracellular signal-regulated kinase in sciatic nerve contributes to neuropathic pain after partial sciatic nerve ligation in mice.
The mitogen-activated protein kinase family plays an important role in several types of pain. However, the detailed role of phosphorylated extracellular signal-regulated kinase (pERK) in the region of injured peripheral nerve is poorly understood. In this study, we investigated whether pERK in injured sciatic nerve contributes to neuropathic pain induced by partial sciatic nerve ligation (PSL) in mice. ⋯ Activation of ERK in Schwann cells of the injured peripheral nervous system may play an important role in the development of neuropathic pain. Our results suggest that pERK itself and ERK-related mediators are potential therapeutic targets for the treatment of neuropathic pain.
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Central sensitization, caused either by tissue inflammation or peripheral nerve injury, plays an important role in persistent pain. An animal model of capsaicin-induced pain has well-defined peripheral and central sensitization components, thus is useful for studying the analgesic effect on two separate components. The focus of this study is to examine the analgesic effects of electroacupuncture (EA) on capsaicin-induced secondary hyperalgesia, which represents central sensitization. ⋯ EA analgesic effect was inhibited by a systemic non-specific opioid receptor (OR) antagonist or an intrathecal mu- or delta-OR antagonist. EA analgesic effect was not affected by an intrathecal kappa-OR antagonist or systemic adrenergic receptor antagonist. This study demonstrates that EA produces a stimulation point-specific analgesic effect on capsaicin-induced secondary hyperalgesia (central sensitization), mediated by activating endogenous spinal mu- and delta-opioid receptors.