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通过Nystrom脊髓后路压迫模型（35．0g／10min）造成脊髓中度损伤，应用激光多普勒血流仪观测了大鼠伤前30min，蛛网膜下腔注射生理盐水及亚硝基左旋精氨酸甲酯（L－NAME）0．15mg、1．5mg三组动物伤后局部脊髓血流的动态变化，并评定了伤后4周神经功能恢复情况。结果发现，L－NAME0.15mg短时间内抑制了脊髓血流，而L－NAME1．5mg较长时间抑制了脊髓血流。4周后L－NAME0．15mg组脊髓功能优于盐水组，而L－NAME1．5mg组脊髓功能较盐水组差。结果提示，适量的L－NAME由于短时间限制了一氧化氮（NO）的释放，有利于神经功能恢复；大剂量的L－NAME由于持续抑制了NO释放而致脊髓损伤加重。
The moderate spinal cord injury was induced by the Nystrom spinal cord posterior compression model (35.0 g / 10 min). Laser doppler flowmetry was used to observe the rats 30 minutes before injury, the subarachnoid injection of normal saline and nitrosyl-levalmin (L-NAME) 0.15mg, 1.5mg three groups of animals after the local spinal cord blood flow dynamic changes, and assessed 4 weeks after injury nerve function recovery. The results showed that, L-NAME0.15mg short-term inhibition of spinal cord blood flow, and L-NAME1.5mg longer inhibited spinal cord blood flow. After 4 weeks, the spinal cord function of L-NAME 0.15 mg group was better than that of saline group, while the spinal cord function of L-NAME 1.5 mg group was worse than that of saline group. The results suggest that appropriate amount of L-NAME is conducive to the recovery of nerve function due to the limited release of nitric oxide (NO) in a short period of time. L-NAME at high dose also aggravates spinal cord injury due to sustained inhibition of NO release.