Articles: hyperalgesia.
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Zhonghua yi xue za zhi · Apr 2011
[Cohort study of remifentanil-induced hyperalgesia in postoperative patients].
To investigate the incidence of remifentanil-induced hyperalgesia and screen for the relevant influencing factors in the post-operative patients. ⋯ Ages under 16 years old, operative duration and remifentanil dose are the risk factors for postoperative remifentanil-induced hyperalgesia. Neither methods of general anesthesia nor operative sites has any effect on the occurrence of hyperalgesia.
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The effects of several potassium (K(+)) channel blockers were studied to determine which K(+) channels are involved in peripheral antinociception induced by the cannabinoid receptor agonist, anandamide. ⋯ This study provides evidence that the peripheral antinociceptive effect of the cannabinoid receptor agonist, anandamide, is primarily caused by activation of ATP-sensitive K(+) channels and does not involve other potassium channels.
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Structural and functional plastic changes in the primary somatosensory cortex (S1) have been observed following peripheral nerve injury that often leads to neuropathic pain, which is characterized by tactile allodynia. However, remodeling of cortical connections following injury has been believed to take months or years; this is not temporally correlated with the rapid development of allodynia and S1 hyperexcitability. Here we first report, by using long-term two-photon imaging of postsynaptic dendritic spines in living adult mice, that synaptic connections in the S1 are rewired within days following sciatic nerve ligation through phase-specific and size-dependent spine survival/growth. ⋯ New spines that generated before nerve injury showed volume decrease after injury, whereas more new spines that formed in the early phase of neuropathic pain became persistent and substantially increased their volume during the late phase. Further, preexisting stable spines survived less following injury than controls, and such lost persistent spines were smaller in size than the surviving ones, which displayed long-term potentiation-like enlargement over weeks. These results suggest that peripheral nerve injury induces rapid and selective remodeling of cortical synapses, which is associated with neuropathic pain development, probably underlying, at least partially, long-lasting sensory changes in neuropathic subjects.
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Oxaliplatin is a key drug for colorectal cancer, but it causes acute peripheral neuropathy (triggered by cold) and chronic neuropathy (sensory and motor neuropathy) in patients. Neurotropin, a non-protein extract from the inflamed rabbit skin inoculated with vaccinia virus, has been used to treat various chronic pains. In the present study, we investigated the effect of neurotropin on the oxaliplatin-induced neuropathy in rats. ⋯ Neurotropin also inhibited the oxaliplatin-induced neurite degeneration in cultured pheochromocytoma 12 (PC12) and rat dorsal root ganglion (DRG) cells. On the other hand, neurotropin did not affect the oxaliplatin-induced cell injury in rat DRG cells. These results suggest that repeated administration of neurotropin relieves the oxaliplatin-induced mechanical allodynia by inhibiting the axonal degeneration and it is useful for the treatment of oxaliplatin-induced neuropathy clinically.
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Evaluating potentially analgesic effects of drugs and various treatments is critically dependent on valid animal models of pain. Since primary somatosensory (SI) cortex is likely to play an important role in processing sensory aspects of pain, we here assess whether monitoring SI cortex nociceptive C fibre evoked potentials can provide useful information about central changes related to hyperalgesia in rats. Recordings of tactile and CO(2)-laser C fibre evoked potentials (LCEPs) in forelimb and hind limb SI cortex were made 20-24h after UV-B irradiation of the heel at a dose that produced behavioural signs of hyperalgesia. ⋯ Tramadol, a centrally acting analgesic known to reduce hyperalgesia, induced changes that counteracted the changes produced by UV-B irradiation on transmission to SI cortex from the hind paw, but had no significant effect on time course of LCEPs from forelimb skin. Tactile evoked potentials were not affected by UV-B irradiation or tramadol. We conclude that altered sensory processing related to hyperalgesia is reflected in altered LCEPs in SI cortex.