Abstract

Objective To investigate the role of central and peripheral sensitization in remifentanil-induced hyperalgesia in a rat model of inflammatory pain. Methods Twenty-one male SD rats weighing 200-300 g were used in this study. Inflammatory pain was induced by intraplantar injection of 1 % carrageenan 100 fd in the left hindpaw in all animals. The animals were then randomly divided into 3 groups ( n = 7 each): control group (group C) and two remifentanil groups (group R1 , R2) . In R1 and R2 groups remifentanil was infused iv at a rate of 10 and 30 μg-kg-1·min-2 respectively starting from 5 min before till 25 min after carrageenan injection, while in group C normal saline was infused iv instead of remifentanil. Bilateral paw withdrawal threshold to mechanical stimulation with von Frey filament (PWT) was measured before (baseline) and at 1 h, 3 h and 1-7 d after carrageenan injection. Bilateral paw withdrawal latency to noxious thermal stimuli (PWL) was measured before and at 2 h, 4 h and 1-7 d after carrageenan injection. The thickness of the plantar surface of left hindpaw was measured before and at 1 h, 4 h and 1-7 d after carrageenan injection. Results Bilateral PWT was significantly lower at day 1 after carrageenan injection in R, and R2 groups than in group C. The right PWT was significantly lower at 2 d and 4-7 d after carrageenan injection in group R2 than in group R, . There was no significant difference in PWL and thickness of the plantar surface of left hindpaw among the 3 groups. Conclusion Central sensitization is involved in developing and maintaining the remifentanil-induced hyperalgesia in a rat model of inflammatory pain, while peripheral sensitization is not. Key words: Hyperalgesia; Central nervous system; Peripheral nerves; Piperidines; Inflammation

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