Articles: hyperalgesia.
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A reduced rectal perceptual threshold has been reported in patients with irritable bowel syndrome (IBS), but this phenomenon may be induced by a comorbid psychological state. We evaluated the rectal pain threshold at baseline and after conditioning (repetitive rectal painful distention: RRD) in patients with IBS or functional abdominal pain syndrome (FAPS), which is an abdominal pain disorder, and in healthy controls, and determined whether rectal hypersensitivity is a reliable marker for IBS. ⋯ Rectal hypersensitivity induced by RRD may be a reliable marker for IBS. Conditioning-induced visceral hypersensitivity may play a pathophysiologic role in IBS.
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Although peripheral nerve function is strongly dependent on energy stores, the role of the mitochondrial electron transport chain, which drives ATP synthesis, in peripheral pain mechanisms, has not been examined. In models of HIV/AIDS therapy (dideoxycytidine), cancer chemotherapy (vincristine), and diabetes (streptozotocin)-induced neuropathy, inhibitors of mitochondrial electron transport chain complexes I, II, III, IV, and V significantly attenuated neuropathic pain-related behavior in rats. While inhibitors of all five complexes also attenuated tumor necrosis factor alpha-induced hyperalgesia, they had no effect on hyperalgesia induced by prostaglandin E2 and epinephrine. ⋯ Neither of these inhibitors, however, affected tumor necrosis factor alpha, prostaglandin E2 or epinephrine hyperalgesia. These experiments demonstrate a role of the mitochondrial electron transport chain in neuropathic and some forms of inflammatory pain. The contribution of the mitochondrial electron transport chain in neuropathic pain is ATP dependent.
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Little is known about the sensory characteristics and underlying mechanisms behind secondary hyperalgesia (HA) (2 degrees HA). The aim of the present study was to investigate the relationships between two different noxious stimuli, mechanical and cold on capsaicin-induced 2 degrees HA. Fourteen healthy volunteers were exposed to three different cold stimuli (20, 10, 0 degrees C) 30 s each, on both forearms. ⋯ Further, 8 min after the injection, the cold stimulation led to an expansion of 2 degrees HA area (from 5.1+/-1.38 to 11.4+/-1.72 cm(2)) to punctuate stimuli distally but not proximally to the injection site (P<0.05). It is concluded that there is no HA to cold stimuli within the area of mechanical 2 degrees HA. However, cooling acts as a conditioning stimulus and expands the area of capsaicin-induced punctuate HA.
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Opioid-induced delayed hyperalgesia and allodynia have been reported in human and animal models. The authors evaluated the influence of different opioids used during clinical anesthesia on nociceptive sensitivity and incisional pain in mice. The role of the inducible nitric oxide synthase on surgical pain and opioid-induced pronociception also was investigated. ⋯ The authors' study demonstrates that the intraoperative administration of fentanyl or remifentanil enhances the extent and duration of postoperative pain. The results suggest a role of the nitric oxide systems in the cause of acute postoperative pain and opioid-induced pronociception.
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Histologic changes in the dorsal root ganglion (DRG) and the nociceptive stimulation thresholds were studied in rats. ⋯ The higher concentration of TNF used induced allodynia and hyperalgesia responses. Because the region showing the histologic changes was significantly larger after application of the higher concentration of TNF, the reaction of the DRG may be related to pain.