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目的为了探讨一氧化氮（NO）在继发性脊髓损伤中的作用机制。方法通过伤前蛛网膜下控注射一氧化氮合成酶（NOS）底物及其不同剂量抑制剂，采用原子吸收分光光度法测定脊髓伤后24h伤段脊髓组织电解质含量和含水量的变化，并观察其超微结构的改变。结果伤前蛛网膜下腔注射NOS底物或大剂量抑制剂均导致伤段脊髓H2O、Na+、Ca2+含量明显升高，K+含量明显降低，且导致脊髓组织超微结构严重紊乱。而注射小剂量NOS抑制剂则导致H2O、Na+、Ca2+含量下降，K+含量升高，并减轻脊髓组织超微结构损害。结论脊髓伤后NO过度释放与抑制均可造成伤段脊髓水、电解质紊乱和组织损害；而NO适当产生则有利于内环境的稳定及脊髓结构完整性的维持。
Objective To explore the mechanism of nitric oxide (NO) in secondary spinal cord injury. METHODS: A nitric oxide synthase (NOS) substrate and its inhibitor were injected subcutaneously before injury and the changes of electrolyte and water content of spinal cord tissue were measured by atomic absorption spectrophotometry Observe the changes in its ultrastructure. Results The pre-injury subarachnoid injection of NOS substrate or high-dose inhibitor resulted in the increase of content of H 2 O, Na + and Ca 2+ in the injured spinal cord and the decrease of K + content, leading to serious disorder of ultrastructure of spinal cord tissue. Injecting small doses of NOS inhibitor led to the decrease of H 2 O, Na + and Ca 2+ contents, increase of K + content, and alleviate the ultrastructure damage of spinal cord tissue. Conclusions Both excessive release of NO and suppression of spinal cord injury can cause water and electrolyte imbalance and tissue damage in the injured spinal cord. However, NO production is beneficial to the stability of the internal environment and the maintenance of spinal structural integrity.