Results 281 to 290 of about 84,168 (327)
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Neural mechanisms of hyperalgesia

Current Opinion in Neurobiology, 1992
Hyperalgesia, or enhanced sensitivity to pain, is a symptom often associated with inflammation, nerve injury and various diseases. Although hyperalgesia appears to be mediated by sensitization of peripheral and central pain-signalling neurons, underlying mechanisms of sensitization are not well understood.
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G2A as a Threshold Regulator of Inflammatory Hyperalgesia Modulates Chronic Hyperalgesia

Journal of Molecular Neuroscience, 2017
Tissue injury, pathogen infection, and diseases are often accompanied by inflammation to release mediators that sensitize nociceptors and further recruit immune cells, which can lead to chronic hyperalgesia and inflammation. Tissue acidosis, occurring at the inflammatory site, is a major factor contributing to pain and hyperalgesia.
Yeu-Shiuan Su   +5 more
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Hyperalgesia and allodynia: peripheral mechanisms

Joint Bone Spine, 2005
Nociceptive signals are generated by peripheral sensory organs called nociceptors, which are endings of small-diameter nerve fibers responsive to the tissue environment. The myriad chemical mediators capable of activating, sensitizing, or arousing nociceptors include kinins, proinflammatory and anti-inflammatory cytokines, prostanoids, lipooxygenases ...
Coutaux, Anne   +3 more
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Ethanol Withdrawal and Hyperalgesia

Current Drug Abuse Reviewse, 2009
Hyperalgesia has been observed during ethanol withdrawal, comparable to the hyperalgesia observed during withdrawal from opioids. To determine the extent of this phenomenon and its potential mechanisms, both behavioral and in vitro studies are examined, and the roles of GABA(A), glutamate and other receptors in mediating the acute and chronic ...
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Opioid-Induced Tolerance and Hyperalgesia

CNS Drugs, 2019
Opioids are very potent and efficacious drugs, traditionally used for both acute and chronic pain conditions. However, the use of opioids is frequently associated with the occurrence of adverse effects or clinical problems. Other than adverse effects and dependence, the development of tolerance is a significant problem, as it requires increased opioid ...
Sebastiano Mercadante   +2 more
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Intravenous Remifentanil Produces Withdrawal Hyperalgesia in Volunteers with Capsaicin-Induced Hyperalgesia

Anesthesia & Analgesia, 2003
Opioids administered during surgery may be beneficial by preempting postoperative pain or detrimental by causing acute tolerance. We used a stable model of hyperalgesia in volunteers to test whether acute opioid exposure also results in such pain sensitization over a period of hours in humans. Ten healthy volunteers were studied.
David D. Hood   +2 more
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Evidence of hyperglycemic hyperalgesia by quinpirole

Pharmacology Biochemistry and Behavior, 1992
Male albino rats were tested for antinociception following injections (IP) with saline, quinpirole (Quin) (1 mg/kg), morphine sulfate (M.S.) (5 mg/kg), or both Quin and M.S. (1 mg/kg and 5 mg/kg, respectively). Quin reduced and M.S. increased tail-flick latency as compared to controls.
Dennis Paul, David S. Roane
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Antagonism of Pain and Hyperalgesia

1979
The purpose of this chapter is to discuss the use of hyperalgesia in the design of assays which quantitatively measure mild analgesic activity. The authors have taken the option not to attempt a comprehensive review of the literature but to comment critically on those contributions which relate directly to this purpose.
James F. Truax   +3 more
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Opioid-induced hyperalgesia

2018
The landmark paper discussed in this chapter is ‘Opioid-induced hyperalgesia: Abnormal or normal pain?’, published by Simonnet and Rivat in 2003. Morphine remains the analgesic of choice for those patients suffering moderate-to-severe pain, but it is increasingly recognized that worsening pain can be associated with chronic opioid consumption—the so ...
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Multiple mechanisms of secondary hyperalgesia

2000
Publisher Summary This chapter discusses the multiple mechanisms of secondary hyperalgesia. The chapter defines the minimal conditions of complexity that must be fulfilled by a model of plasticity of spinal nociceptive transmission in order to explain clinical and psychophysical observations in humans.
Rolf-Detlef Treede, Walter Magerl
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