Articles: hyperalgesia.
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Spinal norepinephrine release and activation of spinal alpha(2)-adrenergic receptors represent important components of descending control of nociception. Recent studies have shown that nitric oxide is capable of stimulating neuronal norepinephrine release in the presence of thiol-containing compounds such as L-cysteine. In the present study, we tested a hypothesis in a rodent model of neuropathic pain that intrathecal injection of the nitric oxide donor S-nitroso-N-acetylpenicillamine and L-cysteine produces an antiallodynic action mediated by the spinal alpha(2)-adrenergic receptors. ⋯ Furthermore, the antiallodynic effect produced by intrathecal injection of a combination of S-nitroso-N-acetylpenicillamine and L-cysteine was abolished by pretreatment with intrathecal injection of a non-specific alpha-adrenergic receptor antagonist, phentolamine, or an alpha(2) receptor antagonist, idazoxan. This study provides the first functional evidence that spinal nitric oxide interacts with the thiol-containing compounds to produce an antiallodynic effect in neuropathic pain. We propose that such an action is mediated by endogenous norepinephrine and spinal alpha(2)-adrenergic receptors.
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The relationship between joint pain and hyperalgesia has been explored in animal models of articular inflammation, but is yet to be shown in the most common rheumatologic condition: osteoarthritis. In this study, cutaneous thermal and mechanical pain thresholds were measured over the thumb of patients with osteoarthritis of the hands. In symptomatic patients, pain was manipulated through resisted active movement of the thumb. ⋯ Increased mechanical sensitivity after exacerbation of MP was alleviated by A beta fiber blockade. It appears that superficial tenderness over the osteoarthritic thumb fluctuates with pain arising from movement of the joint. It is concluded that dorsal horn mechanisms contribute to MP-related hyperalgesia in osteoarthritis of the hands.
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Subcutaneous (s.c.) administration of bee venom into the plantar surface of one hind paw in rats has been found to produce an immediate single phase of persistent spontaneous nociceptive responses (continuously flinching, licking or lifting the injected paw) for 1-2 h accompanied by a 72-96 hour period of primary heat and mechanical hyperalgesia in the injection site and a spread of heat, but not mechanical, hyperalgesia in the non-injected hind paw (Chen et al., 1999b). To gain insight into the underlying mechanisms of the bee venom-induced hyperalgesia in particular, we further identified a heat, but not mechanical, hyperalgesia in an area (paw pad) distant from the injection site induced by s.c. injection of bee venom into the posterior leg 0.8-1.2 cm proximal to the heel measured by paw withdrawal reflex to radiant heat or von Frey monofilament stimuli in conscious rats. ⋯ Moreover, pre- or post-treatment with a single dose of MK-801 (0.01 mg/kg, i.p.), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, completely blocked the occurrence, and reversed the established process of the heat hyperalgesia identified in either the bee venom-treated or non-treated paw pads, while the same treatments with the drug did not produce any influence upon the development and maintaining of the heat and mechanical hyperalgesia identified in the heel of the injected hind limb. Taken together with our previous results following s.c. intraplantar bee venom injection, we conclude that: (1) in addition to the well-identified primary heat and mechanical hyperalgesia in the injection site and its adjacent area, s.c. bee venom is also able to produce a secondary heat hyperalgesia in a region distant from the injection site which has a similar characteristic to the contralateral heat hyperalgesia; (2) NMDA receptors are involved in either development or maintenance of the secondary and the contralateral heat hyperalgesia, but without any role in those processes of the primary heat and mechanical hyperalgesia; (3) the secondary heat hyperalgesia seen in the injected hind limb is likely to share the same neural mechanisms with that identified in the non-injected side via co-activation of NMDA receptors.
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Given that transcutaneous electrical nerve stimulation (TENS) achieves its anti-hyperalgesia through endogenous opioid receptors, this study was undertaken to assess if TENS in combination with morphine was more effective at reducing primary hyperalgesia. Acute inflammation was induced by subcutaneous injection of 3% carrageenan into the rat's hindpaw. The withdrawal latency to heat and the mechanical withdrawal threshold were assessed before and after inflammation and after treatment with TENS (high- or low-frequency). ⋯ In combination with morphine, low-frequency TENS produced a similar reduction in mechanical hyperalgesia when compared with morphine alone. High-frequency TENS in combination with morphine produced a similar reduction in mechanical hyperalgesia when compared with the effects of high-frequency TENS alone. Thus, a lower dose of morphine could be used in combination with TENS to decrease the side effects of systemic morphine and achieve the same degree of analgesia.