Articles: hyperalgesia.
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The platinum derivative oxaliplatin is widely used in colorectal cancer. Its side effects differ from those of the other platinum compounds cisplatin and carboplatin. ⋯ It is believed that HES is the result of peripheral nerve hyperexcitability as a consequence of voltage-gated sodium channel dysfunction, which may be caused by calcium level imbalance. Therapeutic options for HES are the administration of calcium and magnesium, the serotonin and noradrenaline reuptake inhibitor (SNRI) venlafaxine and the thiophosphate amifostine.
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Anesthesia and analgesia · Feb 2008
Case ReportsOpioid-induced hyperalgesia and rapid opioid detoxification after tacrolimus administration.
Opioids can induce central sensitization and hyperalgesia, referred to as "opioid-induced hyperalgesia." Our report describes a patient who underwent intestinal transplant followed by immunosuppressant-related neuropathic pain. Her pain was treated with limited success over the course of 3 yr with different therapies, including i.v. morphine. ⋯ Six months after treatment, she remained opioid free. Our experience suggests that rapid detoxification under general anesthesia may be an effective treatment for opioid-induced hyperalgesia and merits comparison to traditional detoxification methods.
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Electrical stimulation is widely used to assess the function of sensory nerves in humans. In the present study, the threshold current (CT) required to evoke a paw withdrawal response in rats was assessed with stepwise increases in current delivered as sinusoidal stimulation at frequencies of 2000 Hz (CT2000), 250 Hz (CT250) and 5 Hz (CT5). Baseline CT was 840+/-3 microA for CT2000, 267+/-2 microA for CT250 and 165+/-1 microA for CT5 (n=59). ⋯ Intraperitoneal pretreatment with indomethacin (20mg/kg) attenuated carrageenan evoked CT alterations as well as progression of paw swelling and thermal hyperalgesia. In conclusion, low, but not high, frequency stimulation activated a withdrawal response which appears mediated by morphine and capsaicin sensitive primary afferents and this threshold was reduced in the presence of inflammation. These data suggest the validity of such stimulation in defining drug action in a nontissue injurious fashion.
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Brain Behav. Immun. · Feb 2008
Ultra violet-induced localized inflammatory hyperalgesia in awake rats and the role of sensory and sympathetic innervation of the skin.
Exposure to mid range ultrat violet radiations (UVBs) has been shown to produce systemic inflammation and hyperalgesia in mice [Saadé, N. E., Nasr, I. W., Massaad, C. ⋯ Chemical ablation of capsaicin sensitive afferents and guanethidine injection produced significant alteration of the hyperalgesia and allodynia. The increase in cytokine levels by UVB was also altered by both treatments. The present study describes a new animal model for localized UVB-induced inflammatory hyperalgesia and provides evidence about the involvement of neurogenic mechanisms in the observed hyperalgesia and upregulation of proinflammatory mediators.
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Int. Immunopharmacol. · Feb 2008
Role of kinin B1 and B2 receptors in a rat model of neuropathic pain.
Kinin B1 and B2 receptor (R) gene expression (mRNA) is increased in the sensory system after peripheral nerve injury. This study measured the densities of B1R and B2R binding sites in the spinal cord and dorsal root ganglia (DRG) by quantitative autoradiography, and evaluated the effects of two selective non-peptide antagonists at B1R (LF22-0542) and B2R (LF16-0687) on pain behavior after partial ligation of the left sciatic nerve. Increases of B1R binding sites were seen in superficial laminae of the ipsi- and contralateral spinal cord at 2 and 14 days while B2R binding sites were increased on the ipsilateral side at 2 days and on both sides at 14 days. ⋯ At day 21 after sciatic nerve ligation, thermal hyperalgesia was blocked by LF22-0542 (10 mg/kg, s.c.) and LF16-0687 (3 mg/kg, s.c.), yet both antagonists had no effect on tactile and cold allodynia. Data highlight the implication of both kinin receptors in thermal hyperalgesia but not in tactile and cold allodynia associated with peripheral nerve injury. Hence LF22-0542 and LF16-0687 present therapeutic potential for the treatment of some aspects of neuropathic pain.