Spinal actions of NSAIDS in blocking spinally mediated hyperalgesia: the role of cyclooxygenase products.
Recent studies have shown that intrathecal NSAIDs can produce a significant, dose-dependent reduction in the second phase of the formalin response and block thermal hyperalgesia induced by spinally injected N-methyl-D-aspartate and substance P. These observations support the body of literature that indicate that sustained small fiber input yields a hyperalgesia through activation of spinal NMDA and NK1 receptors and that in turn a portion of this action is mediated by the spinal release of cyclooxygenase products.
Yaksh
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Department of Anesthesiology, University of California, San Diego, La Jolla.
Malmberg
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D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D006930:Hyperalgesia / Q000188:drug therapy* / Q000503:physiopathology; D010146:Pain / Q000188:drug therapy* / Q000503:physiopathology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D013116:Spinal Cord / Q000187:drug effects* / Q000201:enzymology / Q000503:physiopathology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D011451:Prostaglandin-Endoperoxide Synthases