摘要
目的：探讨一氧化氮在继发性脊髓损伤中的作用及机制。方法：采用闭合性液压损伤装置致大鼠脊髓（Ｔ９）中度损伤，分别静脉注射生理盐水及一氧化氮合成酶抑制剂Ｌ－ＮＡＭＥ（８，２０，４０ｍｇ／ｋｇ），利用多功能生理仪、手术显微镜、激光多谱勒血流仪、神经肌电图仪分别监测损伤前及后不同时间点平均动脉压、软脊膜小动脉直径、局部血流量、脊髓诱发电位变化、神经行为学评分、组织病理学改变。结果：８ｍｇ／ｋｇＬ－ＮＡＭＥ对大鼠全身血流动力学影响不大，但可促进神经功能恢复；２０ｍｇ／ｋｇＬ－ＮＡＭＥ组神经功能无改善；４０ｍｇ／ｋｇＬ－ＮＡＭＥ明显升高平均动脉压、收缩软脊膜小动脉（９０ｍｉｎ时直径减少１０％）、减少局部血流量（９０ｍｉｎ时减少２２％），局部离子分布紊乱、水肿严重，神经功能障碍不能恢复、甚至加重，体重进行性减轻，死亡率增加。结论：提示一氧化氮在继发性脊髓损伤中，既可起到保护作用又可以起到破坏作用。适当控制一氧化氮生成，有利于组织保护及神经功能恢复。
Objective: To determine the role of nitric oxide during secondary spinal cord injury. Methods: Rats received saline,small dose LNAME (8 mg/kg, 20 mg/kg) and large dose LNAME (40 mg/kg)respectively after close spinal cord modest injury (T9 ) by fluidpercussion model. Then the mean arterial blood pressure (MABP) was recorded with physical machine, the diameter of pial arteriole observed by operation microscope, and the regional blood flow measured by laserDopple flowmetry. The spinal cord somatosensory evoked response was analysed and the neural function of rear leg was evaluated by way of Baffour's. Results: Small dose LNAME had little effects on the hemodynamics but could improve neural function. However,large dose LNAME raised the MABP significantly, constricted pial arteriole(90 min,10%),decreased regional spinal cord blood flow(SCBF)(90 min,22%),augmented the dysfunction of neural system, increased tissue edema,disordered the balance of ion,lost weight and raised the rate of death. Conclusion: Nitric oxide has dual role during secondary spinal cord injury, controls local nitricoxide production suitably, benefits tissue survival and neural function recovery.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
1997年第6期578-581,共4页
Academic Journal of Second Military Medical University
基金
国家自然科学基金
关键词
一氧化氮
一氧化氮合成酶
脊髓损伤
nitric oxide
nitric oxide synthase
spinal cord injuries
