Korean J Anesthesiol.
2003 Jul;45(1):123-132. 10.4097/kjae.2003.45.1.123.
The Effect of alpha2 Adrenergic Agonists and Norepinephrine on Mechanical Allodynia by Freund's Complete Adjuvant Induced Inflammation in Rats
- Affiliations
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- 1Department of Anesthesiology and Pain Medicine, Hanyang University School of Medicine, Seoul, Korea.
- 2Department of Anesthesiology and Pain Medicine, Ulsan University School of Medicine, Seoul, Korea. jhhwang@amc.seoul.kr
- 3Department of Inha University graduate School, Seoul, Korea.
- KMID: 2236748
- DOI: http://doi.org/10.4097/kjae.2003.45.1.123
Abstract
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BACKGROUND: The Freund's complete adjuvant (FCA)-induced inflammation may produce allodynia against a touch stimulus. The antiallodynic effects of brimonidine, a new selective alpha2 receptor agonist, and of rilmenidine, a new more selective imidazoline receptor agonist, have not been evaluated in rats with FCA induced inflammation. Therefore, we investigated the sympathetic component of mechanical allodynia after the development of allodynia secondary to FCA-induced inflammation in rats.
METHODS
A lumbar intrathecal catheter was implantated in male Sprague Dawley rats. Inflammation was induced by the intradermal injection of 0.15 ml FCA under enflurane anesthesia. Using Von Frey filaments, the antiallodynic effects of intrathecal (I.T.) brimonidine (1, 3 microgram), rilmenidine (30, 100 microgram) and saline were examined. In antagonistic study intrathecal yohimbine 30 microgram and rauwolscine 30 microgram were administered to investigate the reversal of the antiallodynic effect by each agonist. We also examined the effects of intradermal norepinephrine followed by I.T. brimonidin, rilmenidine or saline on the withdrawal threshold of rats secondary to allodynia induced by FCA.
RESULTS
I.T. brimonidine or rilmenidine produced dose-dependent antiallodynic effect and which were moderately antagonized by I.T. yohimbine or rauwolscine. Intradermal norepinephrine produced a reduction in the withdrawal threshold in rats.
CONCLUSIONS
Our results suggest that a sympathetic component is likely to be involved in the mechanism of allodynia secondary to FCA-induced inflammation.
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