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REGIONAL ANESTHESIA AND PAIN MEDICINE

The Effect of Diclofenac on the Expression of Spinal Cord c-fos-Like Immunoreactivity After Ischemia-Reperfusion-Induced Acute Hyperalgesia in the Rat Tail

Department of Anaesthesia and Pain Management, The University of Sydney at the Royal North Shore Hospital, St. Leonards, Australia

Address correspondence to Laurence E. Mather, PhD, Department of Anaesthesia and Pain Management, The University of Sydney at the Royal North Shore Hospital, St. Leonards NSW 2065, Australia. Address e-mail to lmather{at}med.usyd.edu.au

Ischemia-reperfusion of the rat tail for 20 min induces local acute hyperalgesia of approximately 1-h duration. We studied how this stimulus affected the expression of c-fos-like immunoreactivity (c-fos-LI) labeling of neurons of the sacral spinal cord, and how diclofenac pretreatment influenced the outcome. After ischemia, the number of c-fos-LI-labeled neurons was significantly increased when assessed at 60, 90, and 120 min after reperfusion (to 183%, 283%, and 164% of control, respectively; all P < 0.01). At 90 min, the number of regional c-fos-LI-labeled neurons was increased to 585% in laminae I-II, 183% in laminae III-IV, 270% in laminae V-X, and 286% in total, compared with respective control values (all P < 0.01). After diclofenac pretreatment (subcutaneous 40 mg/Kg, 30 min before insult) the number of c-fos-LI-labeled neurons at 90 min was increased to 424% in laminae I-II, 150% in laminae III-IV, 142% in laminae V-X, and 183% in total (all P < 0.01). Thus diclofenac pretreatment partially prevented the insult-induced increase in total and regional neuronal c-fos-LI. This acute nociceptive model involves only natural algogens. However, the results were similar to acute chemically induced or chronic adjuvant induced arthritic inflammatory pain models in which increases in c-Fos were partially inhibited by nonsteroidal antiinflammatory drugs.

Implications: This study demonstrates a spinal action of the nonsteroidal antiinflammatory drug, diclofenac, in response to a peripheral insult. Whether the action is caused by reduced peripheral neural activity cannot be ascertained. The action was consistent with a ceiling effect of diclofenac as often found clinically with this class of analgesic drug.