中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2013年
2期
306-308
,共3页
右美托咪定%神经病理性疼痛%一氧化氮%一氧化氮合酶
右美託咪定%神經病理性疼痛%一氧化氮%一氧化氮閤酶
우미탁미정%신경병이성동통%일양화담%일양화담합매
Dexmedetomidine%Neuropathic pain%Nitric oxide%Nitric oxide synthase
目的 观察鞘内注射右美托咪定(DEX)对脊神经结扎(SNL)大鼠大脑皮质中一氧化氮(N0)含量和一氧化氮合酶(NOS)活性的影响,并探讨其作用机制.方法 采用大鼠L5/L脊神经结扎模型,随机分为对照组、假手术组、单纯SNL组、SNL后鞘内注射生理盐水组以及DEX治疗组.每组又据处死大鼠的时间不同而分为3个亚组:术后3、7、14 d组.于大鼠脊神经结扎后不同时间点(3、7、14 d)进行行为学评估后断头处死大鼠.取其大脑皮质,测定NO含量和NOS活性.结果 与对照组和假手术组比较,SNL组机械痛阈降低(3.12±0.71),NO含量、总一氧化氮合酶(TNOS)、诱导型一氧化氮合酶(iNOS)活性在术后3d开始增高(分别为3.14±0.26、11.88±1.62、1.16 ±0.27),一直持续到术后14 d(分别为13.90±2.09、13.90±2.09、1.30±0.35)；与SNL组比较,DEX组机械痛阈升高(9.74±1.48),NO含量、TNOS和iNOS活性明显降低(分别为2.95±0.25、11.84±1.69、0.90±0.15).结论 大鼠大脑皮质中NO、TNOS、iNOS参与了SNL所致神经病理性疼痛的发生,鞘内注射DEX可显著减轻神经病理性疼痛大鼠机械性痛敏,其机制与其抑制脊髓和大脑皮质中NO、TNOS、iNOS的活性有关.
目的 觀察鞘內註射右美託咪定(DEX)對脊神經結扎(SNL)大鼠大腦皮質中一氧化氮(N0)含量和一氧化氮閤酶(NOS)活性的影響,併探討其作用機製.方法 採用大鼠L5/L脊神經結扎模型,隨機分為對照組、假手術組、單純SNL組、SNL後鞘內註射生理鹽水組以及DEX治療組.每組又據處死大鼠的時間不同而分為3箇亞組:術後3、7、14 d組.于大鼠脊神經結扎後不同時間點(3、7、14 d)進行行為學評估後斷頭處死大鼠.取其大腦皮質,測定NO含量和NOS活性.結果 與對照組和假手術組比較,SNL組機械痛閾降低(3.12±0.71),NO含量、總一氧化氮閤酶(TNOS)、誘導型一氧化氮閤酶(iNOS)活性在術後3d開始增高(分彆為3.14±0.26、11.88±1.62、1.16 ±0.27),一直持續到術後14 d(分彆為13.90±2.09、13.90±2.09、1.30±0.35)；與SNL組比較,DEX組機械痛閾升高(9.74±1.48),NO含量、TNOS和iNOS活性明顯降低(分彆為2.95±0.25、11.84±1.69、0.90±0.15).結論 大鼠大腦皮質中NO、TNOS、iNOS參與瞭SNL所緻神經病理性疼痛的髮生,鞘內註射DEX可顯著減輕神經病理性疼痛大鼠機械性痛敏,其機製與其抑製脊髓和大腦皮質中NO、TNOS、iNOS的活性有關.
목적 관찰초내주사우미탁미정(DEX)대척신경결찰(SNL)대서대뇌피질중일양화담(N0)함량화일양화담합매(NOS)활성적영향,병탐토기작용궤제.방법 채용대서L5/L척신경결찰모형,수궤분위대조조、가수술조、단순SNL조、SNL후초내주사생리염수조이급DEX치료조.매조우거처사대서적시간불동이분위3개아조:술후3、7、14 d조.우대서척신경결찰후불동시간점(3、7、14 d)진행행위학평고후단두처사대서.취기대뇌피질,측정NO함량화NOS활성.결과 여대조조화가수술조비교,SNL조궤계통역강저(3.12±0.71),NO함량、총일양화담합매(TNOS)、유도형일양화담합매(iNOS)활성재술후3d개시증고(분별위3.14±0.26、11.88±1.62、1.16 ±0.27),일직지속도술후14 d(분별위13.90±2.09、13.90±2.09、1.30±0.35)；여SNL조비교,DEX조궤계통역승고(9.74±1.48),NO함량、TNOS화iNOS활성명현강저(분별위2.95±0.25、11.84±1.69、0.90±0.15).결론 대서대뇌피질중NO、TNOS、iNOS삼여료SNL소치신경병이성동통적발생,초내주사DEX가현저감경신경병이성동통대서궤계성통민,기궤제여기억제척수화대뇌피질중NO、TNOS、iNOS적활성유관.
Objective To study the effect of dexmedetomidine (DEX) on the content of nitric oxide (NO) and activity of nitric oxide synthase (NOS) in cerebral cortex in rats with neuropathic pain induced by spinal nerve ligation (SNL).Methods Adult Sprague-Dawley male rats were randomly divided into normal control group,sham operation group,SNL group and SNL + DEX group.Every group was subdivided into three sub-groups:3,7 and 14 days postoperation.Mechanical allodynia was represented by 50％ paw withdrawal threshold (PWT).NO content and NOS activity in cerebral cortex were measured by using spectrophotometry.Results As compared with sham operation group and normal control group,50％ PWT of the rats in SNL group was decreased (P ＜ 0.05).As compared with the rats in SNL group,there was an apparent increase of the mean score of 50％ PWT in SNL + DEX group three days later (3.38 ±0.91 vs.5.21 ± 1.54) (P ＜0.05).NOS activity and NO content of the spinal cord were increased significantly in SNL group as compared with those in sham operation group (P ＜ 0.01).NO content,and activity of ttotal nitric oxide synthase(TNOS) and inducible nitric oxide synthase (iNOS) of the spinal cord in SNL + DEX group (2.95 ± 0.25,11.84 ± 1.69 and 0.90 ± 0.15 respectively) were significantly lower than those in SNL group (3.41 ±0.27,13.90 ±2.09 and 1.30 ±0.35 respectively) (P ＜0.05 or P ＜0.01).Conclusion The content of NO and activity of NOS in the spinal cord and cerebral cortex were involved in the mechanism of neuropathic pain.Intrathecal administration of DEX could relieve both mechanical allodynia and cold-induced ongoing pain,which may be associated with the inhibition of the content of NO and activity of NOS in the cerebral cortex.
