Articles: hyperalgesia.
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Recent studies have suggested that glia might play a more active role in synaptic function than previously thought. Therefore, the present studies have evaluated the potential role of spinal cord glia in acute nociceptive processing and in the thermal and mechanical hyperalgesia produced by peripheral injury. In the present experiments, we found that: (1) selective inhibition of glia metabolism with intrathecal (i.t.) administration of fluorocitrate (1 nmol) results in a marked, but reversible, attenuation of the persistent thermal and mechanical hyperalgesia produced by intraplantar zymosan (5 mg); (2) selective inhibition of the inducible form of nitric oxide synthase (iNOS) with i.t. aminoguanidine (1 pmol-1 nmol) resulted in a dose-dependent inhibition of the persistent thermal, but not mechanical hyperalgesia produced by intraplantar zymosan (5 mg); (3) i.t. coadministration of interleukin 1 beta (IL1 beta; 10 ng) and interferon gamma (IFN; 1000 U) resulted in expression of the message for iNOS 8 hr after administration assessed using reverse-transcription polymerase chain reaction (RT-PCR) and Southern blot analysis; and (4) i.t. administration of lipopolysaccharide (LPS; 150 micrograms) produced a time-dependent thermal hyperalgesia compared with saline treated-rats (15 microliters). ⋯ We have previously shown that NO plays a significant role in mechanisms of hyperalgesia. In the present experiments we have extended these observations and have now shown a role for iNOS, expressed by glia, in mechanisms of hyperalgesia. These results suggest an unexplored avenue for the development of potential new and novel therapies for pain control.
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The experimental arthritis of the knee joint used in the present study leads to joint swelling, increased joint temperature, limping, guarding, and a decrease in paw withdrawal latency (PWL) to radiant heat (hyperalgesia) within hours in rats. Unexpectedly, administration of the non-NMDA receptor antagonist, CNQX, in the spinal cord 4 h after initiation of the arthritis significantly reduced the degree of joint inflammation and returned PWL times to baseline. Therefore, the present results indicate that established joint swelling and hyperalgesia can be reduced significantly by CNQX.
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In rheumatology, all of the more than 400 specified syndromes are associated with pain. In the conceptual discussion on the multidimensional influences postulated to explain the development of chronic pain, fibromyalgia has gained increasing interest. Fibromyalgia (fibrositis) is an unspecific soft-tissue disorder with chronic wide-spread musculoskeletal pain and palpable hypersensitivity at fibrositic tender points. ⋯ Histochemical investigations on muscle biopsy and biochemical tests have revealed unspecific changes but no characteristic muscle abnormality. It is supposed that the clinical features may result from central neurohumoral dysfunction combining with peripheral mechanisms to result in hyperalgesia. An integrated therapeutic concept with a reassuring and positive doctor-patient relationship can be helpful in achieving satisfactory treatment results.
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Nerve lesions producing extensive axonal loss can induce painful hyperalgesic states in man. The affect of axonal regeneration and end-organ reinnervation on hyperalgesia and pain is controversial. This study used two axonotmetic models, the sciatic crush injury (CI) and the sciatic chronic constrictive injury (CCI), to investigate the affects of nerve regeneration and reinnervation on hyperalgesia and presumed painful behavior in rats. ⋯ Motor function recovery occurred primarily over days 23-59 post-ligature. During this prolonged period of motor function recovery there was a resolution of the sciatic-mediated plantar surface heat hyperalgesia and the saphenous-mediated heat ANH. The above data support the hypothesis that the successful regeneration of distal axons after axonotmetic lesions can initiate the resolution of neuropathic hyperalgesia.
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Braz. J. Med. Biol. Res. · Aug 1994
The induction of des-Arg9-bradykinin-mediated hyperalgesia in the rat by inflammatory stimuli.
1. The B1 receptor agonist des-Arg9-BK does not induce mechanical hyperalgesia when injected into the rat knee joint at 1-100 nmol, or thermal hyperalgesia when injected intravenously up to 1 mumol/kg. 2. Bradykinin (BK), administered into the joint, (1 nmol-1 mumol) induces a mechanical hyperalgesia, which is maximal by 4 h. ⋯ After interleukin-1 beta pre-treatment (1 unit into the joint or paw) des-Arg9-BK induced both thermal and mechanical hyperalgesia. Co-administration of des-Arg9-Leu8-BK 0.5 nmol with des-Arg9-BK 0.5 nmol into the joint prevented development of hyperalgesia and co-administration of des-Arg9-Leu8-BK (200 nmol/kg, iv) with des-Arg9-BK 10 nmol/kg prevented reduction of thermal withdrawal latencies. 6. These data suggest that after an inflammatory insult B1 receptors may play a role in the transduction of nociceptive information.