Drugs
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Tissue injury or the presence of foreign material initiates a series of pathophysiological events that may manifest as inflammatory pain. The physicochemical characteristics of the initiating factor trigger the release of a unique range of pain mediators that control the threshold and activation of nociceptors. It has been suggested that many nociceptors associated with inflammatory pain are dormant, and are activated by cyclo-oxygenase metabolites and sympathomimetic amines into a state of hyperalgesia. ⋯ The effect of increased cAMP concentrations may be counteracted by stimulation of the arginine/nitric oxide/cGMP pathway. Peripherally acting opiates and dipyrone are examples of analgesics that act via this mechanism. The analgesic effects of glucocorticoids and nimesulide appear to be attributable to inhibition of cytokine release.