目的　探讨一氧化氮 (NO)在戊四唑诱导癫痫中的作用机制。方法　用戊四唑建立大鼠癫痫模型 ,测定癫痫发作后和对照组大鼠大脑皮质、海马中 NO、丙二醛 (MDA)含量及 NO合酶 (NOS)活性。结果　癫痫发作后大脑皮质、海马中 NO、MDA含量及 NOS活性较对照组显著升高 (P<0 .0 5或 P<0 .0 1) ;NO与MDA、NO与 NOS之间呈显著正相关 (两者均 P<0 .0 1)。结论　 NO通过增强脂质过氧化反应在癫痫发作中发挥重要作用 Objective To explore the mechanism of nitric oxide (NO) in pentylenetetrazol induced epilepsy. Methods Rat epilepsy model was established by pentylenetetrazole. The levels of NO, malondialdehyde (MDA) and NO synthase (NOS) in cerebral cortex and hippocampus of rats after epileptic seizure were measured. Results The levels of NO, MDA and NOS in the cerebral cortex and hippocampus were significantly higher than those in the control group (P <0.05 or P <0.01). There were significant positive correlations between NO and MDA, NO and NOS (Both P <0. 01). Conclusion NO plays an important role in seizures by enhancing lipid peroxidation