Background: Primary afferent nociceptor sensitization and its accompanying spontaneous discharge are believed to be the proximate cause of the spontaneous pain and hypersensitivity that follow an acute tissue injury. Evidence for this comes almost entirely from studies limited to the first few minutes to an hour or two after injury, when the inflammatory reaction to injury has just begun. However, there is evidence that inflammatory pain mechanisms differ from acute pain mechanisms and that the mechanisms that drive and modulate inflammatory pain may evolve over time.
Methods: The authors surveyed spontaneous afferent discharge in rats with hind paw inflammation evoked by complete Freund adjuvant over the entire 14 days of the inflammatory pain condition, as determined in parallel experiments assessing allodynia and hyperalgesia.
Results: Inflammation-evoked heat hyperalgesia, mechanoallodynia, and mechanohyperalgesia began within hours, persisted until at least day 7, and resolved by day 14. A large percentage (23%) of A fibers had spontaneous discharge 2 days after inflammation, but the incidence was much reduced (to 7-9%) by 7 and 14 days. At all times, the A-fiber discharge frequency was low (<3.0 Hz) or very low (<0.3 Hz). A large percentage (24%) of C fibers had spontaneous discharge 2 and 7 days after inflammation, but this also declined to near control levels by day 14; C-fiber discharge frequency was also always low (most at 0.3-1.0 Hz). 相似文献
Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix. 相似文献