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Korean J Anesthesiol. 2004 Mar;46(3):336-341. Korean. Original Article.
Park HS , Park JY , Han HC , Lim HJ , Chang SH , Yoon SM .
Department of Anesthesia and Pain Medicine, College of Medicine, Korea University, Seoul, Korea.
Department of Physiology, College of Medicine, Korea University, Seoul, Korea.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are generally attributed to suppression cyclooxygenase enzymes, leading to decreased products of the arachidonic acid cascade. Since the discovery of two isoenzymes of cyclooxygenase, inhibition of cyclooxygenase-2 has been suggested to be responsible for therapeutic effects of NSAIDs without side effects. In the present study, to investigate the extent to peripheral nociception and inflammation of cyclooxygenase-1 and cyclooxygenase-2, diclofenac (non-selective inhibitor), SC-560 (selective cyclooxygenase-1 inhibitor) and NS-398 (selective cyclooxygenase-2 inhibitor) are injected intra-articularly on acute arthritic model in rats. METHODS: Arthritis was induced with 2% lamda-carrageenan (suspended in 50microliter normal saline) into the right knee joint cavity under enflurane anesthesia (2-4%). Before and after the injection, rats were allowed to walk freely through a pathway constructed to record weight load by means of 8 weight sensors (strain gauge type) attached to 8 plates which function independently. The weight load, diameter of both knee joints and weight of rat were measured at each test. At 4 hours and 30 minutes, diclofenac, SC-560 and NS-398 dissolved in 10% dimethyl sulfoxide were injected intra-articularly (50microgram/50microliter). RESULTS: The weight loads increased in diclofenac group at 6 and 9 hours and in NS-398 group at 24 and 48 hours after induction of arthritis. The diameter ratio decreased in diclofenac group at 12 hours after induction of arthritis. CONCLUSIONS: These results suggest that peripheral nociception and inflammation in acute model of arthritis in rats are likely related with both cyclooxygenase-1 and cyclooxygenase-2 pathways.

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