Articles: hyperalgesia.
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This study examined the effect of repeated intradermal capsaicin injections on capsaicin pain intensity and areas of allodynia and punctate hyperalgesia. Seventeen healthy volunteers participated in four sessions separated by at least 5 days. Each session included four intradermal injections of 10 microg of capsaicin. ⋯ There were no significant relations between capsaicin pain intensity and areas of allodynia and punctate hyperalgesia after first injections. The findings indicate that the response to intradermal injection of capsaicin is dependent on the time and distance between injections. The lack of significant relation between capsaicin pain intensity and area of allodynia and punctate hyperalgesia suggests that the two phenomena are mediated by different central mechanisms.
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Given that transcutaneous electrical nerve stimulation (TENS) achieves its anti-hyperalgesia through endogenous opioid receptors, this study was undertaken to assess if TENS in combination with morphine was more effective at reducing primary hyperalgesia. Acute inflammation was induced by subcutaneous injection of 3% carrageenan into the rat's hindpaw. The withdrawal latency to heat and the mechanical withdrawal threshold were assessed before and after inflammation and after treatment with TENS (high- or low-frequency). ⋯ In combination with morphine, low-frequency TENS produced a similar reduction in mechanical hyperalgesia when compared with morphine alone. High-frequency TENS in combination with morphine produced a similar reduction in mechanical hyperalgesia when compared with the effects of high-frequency TENS alone. Thus, a lower dose of morphine could be used in combination with TENS to decrease the side effects of systemic morphine and achieve the same degree of analgesia.
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Several lines of evidence have shown a role for the nitric oxide/cyclic guanosine monophosphate signaling pathway in the development of spinal hyperalgesia. However, the roles of effectors for cyclic guanosine monophosphate are not fully understood in the processing of pain in the spinal cord. The present study showed that cyclic guanosine monophosphate-dependent protein kinase Ialpha but not Ibeta was localized in the neuronal bodies and processes, and was distributed primarily in the superficial laminae of the spinal cord. ⋯ Moreover, cyclic guanosine monophosphate-dependent protein kinase Ialpha protein expression was dramatically increased in the lumbar spinal cord 96 h after injection of formalin into a hindpaw, which occurred mainly in the superficial laminae on the ipsilateral side of a formalin-injected hindpaw. This up-regulation of cyclic guanosine monophosphate-dependent protein kinase Ialpha expression was completely blocked not only by a neuronal nitric oxide synthase inhibitor, 7-nitroindazole, and a soluble guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, but also by an N-methyl-D-aspartate receptor antagonist, dizocilpine maleate (MK-801). The present results indicate that noxious stimulation not only initially activates but also later up-regulates cyclic guanosine monophosphate-dependent protein kinase Ialpha expression in the superficial laminae via an N-methyl-D-aspartate-nitric oxide-cyclic guanosine monophosphate signaling pathway, suggesting that cyclic guanosine monophosphate-dependent protein kinase Ialpha may play an important role in the central mechanism of formalin-induced inflammatory hyperalgesia in the spinal cord.