European journal of pain : EJP
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Spironolactone, a commonly used mineralocorticoid receptor antagonist, has been reported to potentiate the effect of morphine in the rat. The aim of this study was to investigate the effects of spironolactone on morphine antinociception and tissue distribution. ⋯ Spironolactone has no antinociceptive effects in thermal models of pain, but it enhances the antinociceptive effects of morphine mainly by increasing morphine central nervous system concentrations, probably by inhibiting P-gp.
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Cold allodynia and cold hyperalgesia are both elusive features of neuropathic pain, particularly in patients with various polyneuropathies. Numerous studies have suggested that topical application of L-menthol causes temporary cold hypersensitivity and thus acts as a proxy for associated symptoms. This review summarizes studies on L-menthol-induced nociception, cold allodynia and cold hyperalgesia in vitro, in animals and in humans. ⋯ Topical high-concentration L-menthol consistently induces cold hypersensitivity in animals and humans, thus constituting a predictable surrogate model of cold allodynia and hyperalgesia. Understanding translational features of this model and its underlying mechanisms could be valuable in preclinical and human phases of drug development and in improving current treatment of patients with polyneuropathy.
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Annexin 1, a glucocorticoid (GC)-inducible protein, can play an important role via formyl peptide receptor like 1 (FPR2/ALX, also known as FPRL1) in inflammatory pain modulation. The aim of this review is to analyze different lines of evidence for the role of ANXA1 with different mechanisms on inflammatory pain and describe the profile of ANXA1 as a potential analgesic. A Medline (PUBMED) search using the terms 'Annexin 1 distribution OR expression, FPR2/ALX distribution OR expression, Annexin 1 AND pain, Annexin 1 AND FPR2/ALX AND pain' was performed. ⋯ The antinociception of ANXA1 has been evaluated in diverse pain models. It has been suggested that ANXA1 may exerts its action via: (1) inhibiting vital cytokines involved in pain transmission, (2) inhibiting neutrophil accumulation through preventing transendothelial migration via an interaction with formyl peptide receptors, (3) facilitating tonic opioid release from neutrophil in inflammatory site, (4) interrupting the peripheral nociceptive transmission by suppressing neuronal excitability. In general, ANXA1 is a potential mediator for anti-nociception and the role with its receptor constitute attractive targets for developing anesthesia and analgesic drugs, and their interaction may prove to be a useful strategy to treat inflammatory pain.
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High-frequency electrical stimulation (HFS) of the human forearm evokes analgesia to blunt pressure in the ipsilateral forehead, consistent with descending ipsilateral inhibitory pain modulation. The aim of the current study was to further delineate pain modulation processes evoked by HFS by examining sensory changes in the arm and forehead; investigating the effects of HFS on nociceptive blink reflexes elicited by supraorbital electrical stimulation; and assessing effects of counter-irritation (electrically evoked pain at the HFS-conditioned site in the forearm) on nociceptive blink reflexes before and after HFS. ⋯ These findings suggest that HFS concurrently triggers hemilateral inhibitory and facilitatory influences on nociceptive processing over and above more general effects of counter-irritation. The inhibitory influence may help limit the spread of sensitization in central nociceptive pathways.
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Microvascular dysfunction and ischaemia in muscle play a role in the development of cutaneous tactile allodynia in chronic post-ischaemia pain (CPIP). Hence, studies were designed to assess whether pentoxifylline (PTX), a vasodilator and haemorrheologic agent, relieves allodynia in CPIP rats by alleviating microvascular dysfunction. ⋯ Since poor tissue perfusion underlies early stages of CPIP pain, the ameliorative effect of PTX on microvascular dysfunction might account for its anti-allodynic effect in our experimental model of complex regional pain syndrome type I.