Articles: opioid-analgesics.
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Postoperative pain arises largely from distension and sectioning of nerve fibers, which generate a short-lasting but enormous afferent impulse barrage. This causes a long-lasting enlargement of receptive fields and an increase in excitability of dorsal horn neurons sending their axons up to the brain. ⋯ Prostaglandins in the spinal cord facilitate the synaptic transmission from nociceptive afferents. Nonsteroidal anti-inflammatory drugs (NSAIDs) produce relief from postoperative pain by blocking the formation of prostaglandins in the spinal cord, thus abolishing the facilitatory effect of these compounds.
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The description of multiple classes of opioid receptors has had a major impact on our understanding of the mechanisms of analgesia. Three major classes of opioid receptors have been defined: mu, kappa, and delta. The mu receptors have been further subclassified into two distinct subtypes (mu 1 and mu 2), as have the delta receptors (delta 1 and delta 2). ⋯ In addition to their ability to act independently, the various systems also interact synergistically with each other. Thus, the relief of pain involves the complex interaction of at least six receptor systems. This review discusses the implications of opiate receptor multiplicity on the control of pain.
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Spinal administration of morphine and other opiates has been used in clinical practice since many years, particularly in the outpatient management of cancer pain patients. The rationale and the safety of chronic spinal opiate administration is well established and not questioned anymore. However, the indications to use these therapies remain unclear, essentially because no controlled studies have ever shown the advantages of these treatments. ⋯ This raises technological and financial issues, as well as management problems related to the home care system. The choices that have to be made should include the home physician, the home care nursing team as well as the hospital based pain management team. This short overview will deal with some of these aspects.
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Ann Fr Anesth Reanim · Jan 1993
ReviewMechanisms of activation of human mast cells and basophils by general anesthetic drugs.
A study was performed about the effects of increasing concentrations of muscle relaxants (suxamethonium, d-tubocurarine, vecuronium, and atracurium), hypnotics (propofol, ketamine, and thiopental), opioids (morphine, buprenorphine, and fentanyl), and benzodiazepines (diazepam, flunitrazepam, and midazolam) on the release of preformed (histamine and tryptase) and de novo synthesized (prostaglandin D2: PGD2 and peptide-leukotriene C4: LTC4) chemical mediators from human basophils and mast cells isolated from skin (HSMC), lung parenchyma (HLMC) and heart tissue (HHMC). None of the drugs tested induced the release of histamine or LTC4 from basophils of normal donors. Suxamethonium did not induce mediator release from any type of human mast cell tested. ⋯ Diazepam and flunitrazepam only induced a small release of histamine from mast cells, whereas midazolam caused the release of histamine from HLMC. The biochemical pathways underlying the release of mediators from human mast cells induced by drugs used during general anaesthesia are different from those underlying the immune release of histamine. From the results obtained with the in vitro model described here, it is clear that new drugs promising for the anesthesiologic arena should be tested in vitro before their potential histamine-releasing activity is experienced in vivo.