Articles: hyperalgesia.
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Acta Anaesthesiol Scand · Sep 2001
Randomized Controlled Trial Clinical TrialEffect of naloxone on primary and secondary hyperalgesia induced by the human burn injury model.
Opioid antagonists may change the responses in models of experimental hyperalgesia. This indicates a possible involvement of the endogenous opioid system in these models. The aim of the present study was to evaluate whether activation of the endogenous opioid system could be demonstrated in the human burn injury model of cutaneous hyperalgesia, using an intravenous challenge with the non-selective opioid antagonist naloxone. ⋯ Activation of an endogenous opioid response following induction of hyperalgesia in human volunteers by a burn injury could not be demonstrated with an intravenous naloxone challenge. These findings suggest that the endogenous opioid response is not a confounding factor in this model.
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We examined the effects of intrathecally preadministered injections of a phosphorothioate analog of c-fos antisense and mismatch oligodeoxynucleotides (ODNs) on the withdrawal latency to a thermal stimulus following unilateral injection of complete Freund's adjuvant (CFA) into the hind footpad of rats. Pretreatment with the c-fos antisense ODN significantly decreased the CFA-induced expression of c-Fos protein dose-dependently in ipsilateral laminae I/II (LI/II) of the dorsal horn (mean +/- SEM per section: 10 nM ODN, 43.9+/-1.3; 25 nM ODN, 19.4+/-4.1) compared with pretreatment with the mismatch ODN (63.6+/-2.9; 60.6+/-4.0) or saline (56.6+/-5.5). ⋯ Pretreatment with 10 nM antisense ODN had a less significant effect. These results indicate that the expression of CFA-induced c-Fos in the dorsal horn might facilitate thermal nociception.
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1. Using the rat paw pressure test, in which increased sensitivity is induced by intraplantar injection of prostaglandin E2, we studied the action of several K(+) channel blockers in order to determine what types of K(+) channels could be involved in the peripheral antinociception induced by dibutyrylguanosine 3 : 5'-cyclic monophosphate (DbcGMP), a membrane permeable analogue of cyclic GMP. 2. DbcGMP elicited a dose-dependent (50, 75, 100 and 200 microg paw(-1)) peripheral antinociceptive effect. ⋯ Charybdotoxin (2 microg paw(-1)), a selective blocker of high conductance Ca(2+)-activated K(+) channels, and apamin (10 microg paw(-1)), a selective blocker of low conductance Ca(2+)-activated K(+) channels, did not modify the peripheral antinociception induced by DbcGMP. 5. Tetraethylammonium (2 mg paw(-1)), 4-aminopyridine (200 microg paw(-1)) and cesium (800 paw(-1)), non-selective voltage-gated potassium channel blockers, also had no effect. 6. Based on this experimental evidence, we conclude that the activation of ATP-sensitive K(+) channels could be the mechanism by which DbcGMP induces peripheral antinociception, and that Ca(2+)-activated K(+) channels and voltage-dependent K(+) channels appear not to be involved in the process.
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To review the pathophysiology of fibromyalgia syndrome. ⋯ Multiple abnormal findings in fibromyalgia patients strongly indicate a neuropathic pain syndrome, reminiscent of complex regional pain syndrome or postherpetic neuralgia. In addition, fibromyalgia syndrome seems to share similar characteristics with these neuropathic pain syndromes, including ineffective response to many analgesics.
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Reg Anesth Pain Med · Sep 2001
Randomized Controlled Trial Clinical TrialEffect of systemic adenosine on pain and secondary hyperalgesia associated with the heat/capsaicin sensitization model in healthy volunteers.
Adenosine is an endogenous compound that may have analgesic effects. Results from clinical trials are not consistent, however, and there is a need for large-scale, randomized, placebo-controlled studies to clarify the role of adenosine in the treatment of pain states, including acute nociceptive pain and pain involving central sensitization. ⋯ We conclude that adenosine has no effect on acute nociceptive pain induced by heat stimulation or on secondary hyperalgesia induced by heat/capsaicin sensitization in healthy volunteers.