Articles: hyperalgesia.
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Comparative Study
Comparison of the effects of ureteral calculosis and occlusion on muscular sensitivity to painful stimulation in rats.
An animal model of muscular hyperalgesia was developed. In humans, this disorder follows painful crises due to ureteral calculosis. Changes in vocalization thresholds to electrical stimulation of the obliquus externus muscle of both sides were studied in a group of rats with chronically implanted muscles before and after the production of a stone in one ureter. ⋯ Ligature alone never induced any hyperalgesic effect. Stone plus ligature produced a marked hyperalgesia (max 39%) in the ipsilateral muscle, which lasted for only 5 days. It is concluded that the ureteral stone is the factor responsible for the appearance of muscular hyperalgesia.
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Neuroscience letters · Jul 1990
A-fibers mediate mechanical hyperesthesia and allodynia and C-fibers mediate thermal hyperalgesia in a new model of causalgiform pain disorders in rats.
Unilateral tight ligation of about half of the sciatic nerve in rats rapidly produces sympathetically dependent neuropathic pain which lasts many months and resembles causalgia in humans. The sensory abnormalities detected at the plantar side of the hindpaws include: (1) nocifensive responses to repetitive light touch (allodynia); (2) bilateral reduction in withdrawal thresholds to repetitive von-Frey hair stimulation (mechanical hyperesthesia); (3) bilateral reduction in withdrawal thresholds to CO2 laser heat pulses; and (4) unilateral increase in response duration to an intense laser heat pulse (thermal hyperalgesia). Using neonatal capsaicin treatment, we determined the type of afferent fiber remaining in the partially injured nerve, which mediates these disorders. ⋯ These disorders were, therefore, mediated by myelinated fibers. In contrast, thermal hyperalgesia failed to develop in capsaicin-treated rats following partial nerve injury. Thus, thermal hyperalgesia produced by partial nerve injury appears to be mediated by heat-nociceptive C-fibers.
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The intradermal injection of adenosine produces a dose-dependent decrease in mechanical nociceptive threshold in the hindpaw of the rat that is not attenuated by elimination of indirect pathways for the production of hyperalgesia. Adenosine-induced hyperalgesia is mimicked by the A2-agonists, 5'-(N-ethyl)-carboxamido-adenosine and 2-phenylaminoadenosine but not by the A1-agonist, N6-cyclopentyladenosine and antagonized by the adenosine A2-receptor antagonist, PD 081360-0002 but not by the A1-antagonist, 1,3-dipropyl-8-(2-amino-4-chlorophenyl)xanthine. ⋯ However, 1-acetyl-2-(8-chloro-10,11-dihydrodibenz[b,f]oxazepine-10-ca rbonyl) hydrazine, a prostaglandin-receptor antagonist, inhibits prostaglandin E2 (Taiwo and Levine, Brain Res. 458, 402-406, 1988) but not 2-phenylamino-adenosine hyperalgesia and PD 081360-0002, the adenosine receptor antagonist, inhibits 2-phenylamino-adenosine but not prostaglandin E2 hyperalgesia. These data suggest that adenosine is a directly acting agent that produces hyperalgesia by an action at the A2-receptor and that this hyperalgesia is mediated by the cAMP second messenger.
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Quantitative thermal and mechanical algometry was studied in 4 human subjects exposed to various concentrations of capsaicin administered topically to the skin of the palm or forearm. Treated skin patches were assessed for changes in heat pain threshold and in mechanical pain threshold at various controlled temperatures. The results showed that: (1) in addition to heat hyperalgesia, capsaicin consistently induces overt mechanical hyperalgesia; (2) thermal and mechanical hyperalgesias are linearly dependent on the log of capsaicin dose; (3) mechanical hyperalgesia is increased by increasing skin temperature; (4) mechanical hyperalgesia is abolished by cooling the skin to a point about 10 degrees C below the threshold for heat pain, a temperature that does not impair touch or sharp pain sensation. ⋯ Hyperalgesia is also transiently depressed for at least 30 min during the postischaemic period, well beyond the duration of paraesthesiae or overt hyperaemia. Sensory changes identical to those induced experimentally by capsaicin have been observed in patients with a particular variety of neuropathic pain (ABC syndrome) and have been termed polymodal hyperalgesia and cross modality threshold modulation (Ochoa, 1986; Ochoa et al., 1987). Based on these overall observations, it is postulated here that the sensory abnormalities induced by capsaicin and those observed in this particular variety of patients relate to primary hyperalgesia and share a common mechanism in that the excitable receptor membrane of polymodal C nociceptors behaves as if it 'misreads' temperature.