Effect of N-acetyl-cysteine on Allodynia in a Chronic Post-ischemia Pain Model of Rat

ABSTRACT

BACKGROUND: Complex regional pain syndrome type I (CRPS-I) is a clinical syndrome that is poorly understood and difficult to treat. Reactive oxygen species (ROS) and inflammatory responses may contribute to the development of CRPS-I. This study evaluated the effect of N-acetyl-cysteine (NAC) on both mechanical and cold allodynia in a rat CRPS-I model. METHODS: Male adult SD rats were used for the CRPS-I model that was produced following prolonged hindpaw ischemia/reperfusion. The rats were divided into 3 groups, Group O (-) (n = 8) rats without a tourniquet; Group O (+) (n = 8) rats received ischemic injury with a tourniquet on the hindpaw and they were reperfused 3 hours after the tourniquet application; and Group ON (+) (n = 8) rats received ischemic injury with a tourniquet ring on the hindpaw and they were reperfused 3 hours after the tourniquet application and they received intraperitoneal N-cetyl-ysteine (500 mg/kg) injection just after the tourniquet application and at 1 day and 2 days after the reperfusion. RESULTS: In the Group O (+), mechanical (von Frey hair) and cold (acetone exposure) allodynia were evident in the affected hindpaw as early as 1 day after reperfusion; this was extended for 2 weeks and it spread to the uninjured contralateral hindpaw. In the Group ON (+), the mechanical and cold allodynia were attenuated compared to those rats of Group O (+). CONCLUSIONS: NAC, a free radical scavenger, was able to reduce mechanical and cold allodynia in this model, and the generation of ROS is partly responsible for CRPS-I.