目的　研究神经元型一氧化氮合酶(NOS)抑制剂 7 硝基吲唑(7-nitroindazole,7-NI)在新生大鼠缺氧缺血性脑损伤(hypoxic ischemic brain damage,HIBD)中的作用机制。　方法　将 54只新生7日龄Wistar大鼠随机分为假手术组、HIBD组和 7-NI治疗组;其中后两组各再分为四个时点(1、2、6、8 h),检测不同时点结扎侧脑组织中NOS、一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)水平的变化。另 18 只新生大鼠随机分为假手术组、HIBD 组和 7-NI 组,每组 6 只,应用TUNEL法观察7 NI对 HIBD 后 24 h 神经细胞凋亡的影响。　结果　假手术组 NOS(1. 555±0.223) U/mg;NO (0. 749±0. 135)μmol/g; SOD(24. 184±1. 446) nU/mg; MDA(1. 319±0. 282)nmol/mg;HIBD组NOS 1 h (3.345±0.367) U/mg , 8 h (4.469±0.275) U/mg ;NO 1 h (2.419±0.254)μmol/g,8 h (3. 556±0. 309)μmol/g; SOD 1 h (22. 052±1. 179) nU/mg, 8 h (17. 124±1.541) nU/mg;MDA 1 h (2.449±0.418) nmol/mg,8 h (4.576±0.294) nmol/mg;7 NI组NOS 1 h(1.606±0.149) U/mg,8 h (2.917±0.426) U/mg ;NO 1 h (0.879±0.169)μmol/g,8 h (1.803±0.275)μmol/g;SOD 1 h (24.045±1.219) nU/mg ,8 h (20.688±1.696) nU/mg ;MDA 1 h (1.569±0. Objective To investigate the effect of 7-nitroindazole (7-NIH), a neuronal nitric oxide synthase inhibitor, on hypoxic ischemic brain damage (HIBD) in neonatal rats Mechanism. Methods 54 neonatal 7-day-old Wistar rats were randomly divided into sham operation group, HIBD group and 7-NI treatment group. The latter two groups were further divided into four time points (1, 2, 6, 8 h) The changes of NOS, nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) in the ligation group were detected at different time points. Another 18 neonatal rats were randomly divided into sham-operation group, HIBD group and 7-NI group, with 6 rats in each group. TUNEL method was used to observe the effect of 7 NI on neuronal apoptosis at 24 h after HIBD. Results NOS (1.555 ± 0.223) U / mg, NO (0.749 ± 0.135) μmol / g, SOD (24.184 ± 1.446) nU / mg, 0.82) nmol / mg in the HIBD group, NOS 1 h (3.345 ± 0.367) U / mg, 8 h (4.469 ± 0.275) U / mg and NO 1 h (2.419 ± 0.254) μmol / g, 556 ± 0. 309) μmol / g, SOD 1 h (22. 052 ± 1.179 nU / mg, 8 h (17.124 ± 1.541) nU / mg and MDA 1 h (2.449 ± 0.418) nmol / , And 8 h (4.576 ± 0.294) nmol / mg respectively. In the NI group, NOS 1 h (1.606 ± 0.149) U / mg and 8 h (2.917 ± 0.426) U / (1.803 ± 0.275) μmol / g for 8 h, SOD1 h (24.045 ± 1.219) nU / mg, 8 h (20.688 ± 1.696) nU / mg and MDA for 1 h