Articles: hyperalgesia.
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Objective. This experiment was performed to test the hypothesis that intrathecally pumped saline, but not artificial cerebrospinal fluid (CSF), would be analgesic in a rat model of neuropathic pain. Materials and Methods. ⋯ No analgesia was observed on tests of spontaneous pain or pressure hyperalgesia (p > 0.1). Conclusions. Intrathecally pumped saline and artificial CSF have analgesic effects on some neuropathic and normal, nociceptive pain signs in CCI rats.
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Anesthesia and analgesia · Oct 2002
Randomized Controlled Trial Clinical TrialThe effect of chronic oral desipramine on capsaicin-induced allodynia and hyperalgesia: a double-blinded, placebo-controlled, crossover study.
The tricyclic antidepressants are often used for the treatment of neuropathic pain. In this study, we evaluated one of these drugs on human cutaneous experimental pain. A randomized, double-blinded, placebo-controlled, crossover design methodology was conducted. Subjects participated in 2 14-day study sessions separated by a 7-day washout period. One session was with desipramine and one with placebo. At baseline, Day 7, and Day 15, quantitative sensory testing was performed to thermal and mechanical stimuli. On Day 15 only, intradermal capsaicin was injected on the volar aspect of the forearm followed by an assessment of pain and hyperalgesia. Oral desipramine had no significant effect on acute sensory thresholds, pain, secondary hyperalgesia, or flare response induced by intradermal capsaicin. Mean peak plasma levels of desipramine were within the therapeutic range for the treatment of depression. This study further supports a lack of effect of the tricyclic antidepressants on acute nociception and experimentally-induced secondary hyperalgesia. ⋯ Human experimental pain models have recently been developed; however, the efficacy of the tricyclic antidepressants (TCA) in these models has not been systematically studied. This investigation provides further validation of human experimental pain models and demonstrates that the chronic delivery of a TCA has no effect on human experimental pain.
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Plasticity in the spinal dorsal horn may underlie the development of chronic pain following peripheral nerve injury or inflammation. In this study, we examined whether chronic constriction injury of the sciatic nerve was associated with changes in the immunoreactive content of cyclic AMP response element binding protein (CREB), protein kinase A (PKA), and calcineurin Aalpha and Abeta in the spinal dorsal horn. In animals exhibiting thermal hyperalgesia as a behavioral sign of neuropathic pain 7 days after loose ligation of the sciatic nerve (chronic constriction injury), there was a significant increase in the content of phosphorylated (activated) CREB (pCREB). ⋯ In contrast, there were no differences in the content of non-phosphorylated CREB, and phosphorylated or non-phosphorylated PKA between control and sciatic ligation animals either 7 or 28 days after surgery. These data established a close association in the expression of thermal hyperalgesia with CREB activation and decreased calcineurin content in the spinal dorsal horn. The data revealed a significant but reversible shift in the manner in which spinal neurons processed sensory information following peripheral nerve injury, and lent further support to the notion that plasticity in the spinal dorsal horn may have contributed to the development of chronic pain.
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This study was designed to determine whether intrathecal octreotide (sandostatin), a synthetic octapeptide derivative of somatostatin, relieved thermal hyperalgesia and reduced the evoked spinal c-Fos expression in rats with chronic constriction injury (CCI) of the sciatic nerve. Intrathecal catheters were implanted in rats 7 days before CCI of the sciatic nerve over the left hind limb. After confirmation of the development of thermal hyperalgesia by decreased paw withdrawal latencies (PWL) to heat stimulation 7 days after CCI, intrathecal sandostatin at 20, 40, and 80 microg was administered, respectively. ⋯ Expression of Fos-LI neurons in the 80 microg group was nearly completely inhibited. These data suggest that intrathecal sandostatin significantly relieved thermal hyperalgesia behaviorally but with limited effects and dose-dependently reduced spinal Fos-LI neurons expression evoked by stroking stimulation, which may reflect mechanical allodynia in rats with sciatic constriction injury. This implies that intrathecal sandostatin was effective in the treatment of neuropathic pain.
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European cytokine network · Oct 2002
Cytokine-induced neutrophil chemoattractant 1 (CINC-1) mediates the sympathetic component of inflammatory mechanical hypersensitivitiy in rats.
The hyperalgesic effect of cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL1) was measured in a model of mechanical hyperalgesia in rats. CINC-1 evoked a dose-dependent mechanical hypersensitivity, which was already significant 2 h after the cytokine injection, peaked 4 h after and decreased thereafter. The local pre-treatment of the rats with the beta-adrenoceptor antagonist, atenolol (25 microg paw-1), but not with the cyclooxygenase inhibitor indomethacin (100 microg paw-1), inhibited (86%) the CINC-1-induced hypersensitivity. ⋯ The association of both antisera abolished the hypersensitivity effect of carrageenin and TNF-alpha. In addition, carrageenin, LPS and TNF-alpha were shown to stimulate the production of immunoreactive CINC-1 in the skin of injected paws. These data suggest that CINC-1, released at sites of inflammation, mediates inflammatory hyperalgesia in rats via release of sympathomimetic amines.