Reactive oxygen species and N-methyl-D-aspartate receptor-mediated central sensitization in hindlimb ischemia/reperfusion injury-induced neuropathic pain rats.
10.4097/kjae.2009.56.2.186
- Author:
Kwang Woo KIM
1
;
Mi Jin HA
;
Kyung Young JUNG
;
Kyung Hwa KWAK
;
Sung Sik PARK
;
Dong Gun LIM
Author Information
1. Soo Pain Clinic, Busan, Korea.
- Publication Type:Original Article
- Keywords:
Allodynia;
Neuropathic pain;
Superoxide
- MeSH:
Adult;
Animals;
Blotting, Western;
Central Nervous System Sensitization;
Cytochromes c;
Hindlimb;
Humans;
Hyperalgesia;
Ischemia;
Kinetics;
Male;
Models, Animal;
N-Methylaspartate;
Neuralgia;
Plasma;
Rats;
Reactive Oxygen Species;
Reperfusion;
Spinal Cord;
Superoxides;
Xanthine;
Xanthine Oxidase
- From:Korean Journal of Anesthesiology
2009;56(2):186-194
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Reactive oxygen species (ROS) contribute to development of neuropathic pain. A neuropathic pain syndrome was produced in rats following prolonged hindpaw ischemia/reperfusion injury, creating an animal model of complex regional pain syndrome-Type I (CRPS-I). This study was designed to evaluate the validity of this model for ROS and pain research. Herein we show superoxide produces N-methyl-D-aspartate (NMDA) mediated mechanical allodynia. METHODS: Male adult SD rats were used for neuropathic pain model. Plasma superoxide production rates of before ischemia (BI) and 5 min after reperfusion (JR) were measured via cytochrome C reduction in the presence of xanthine (without xanthine oxidase, kinetics, 550 nm). Mechanical allodynia was measured in both hindpaws. Activation of NMDA receptor subunit 1 (P-NR1) of lumbar spinal cord (L4-L6) in accordance with the change of allodynia was analyzed by the Western blot. RESULTS: Allopurinol-inhibitable, xanthine oxidase-mediated plasma superoxide production was increased at AR. Mechanical allodynia was present in both hindpaws as early as 1 hr after reperfusion, and lasted at least 1 week. The expression of P-NR1 was the highest at 3 days after reperfusion when the withdrawal threshold was the lowest point. SOD significantly blocked P-NR1 activation. CONCLUSIONS: This study suggests that ischemia/reperfusion injury induced neuropathic pain model is a good candidate for the research fields of ROS and pain mechanism. The generation of ROS, especially superoxide is partly responsible for NMDA-mediated mechanical allodynia.
