中文摘要：

目的 探讨氢气治疗对急性脑缺血再灌注损伤大鼠海马NO和一氧化氮合酶（NOS）的影响.方法 选择SD大鼠72只,随机分为3组：假手术组、模型组和治疗组（腹腔注射2%氢气饱和生理盐水）,每组24只,每组又分为6、24 h 2个时间点.采用线栓法制作大鼠大脑中动脉缺血再灌注模型.免疫组织化学方法测定海马NOS的表达;硝酸还原酶法测定海马组织匀浆中NO含量;NOS检测试剂盒检测海马组织提取液中NOS的活性.结果 模型组治疗6 h海马NOS阳性细胞、NO含量及NOS活性明显高于假手术组,而治疗组上述指标较模型组明显下降（P〈0.05）;模型组治疗24 h海马NOS阳性细胞、NO含量及NOS活性明显高于假手术组,差异有统计学意义（P〈0.05）,但治疗组与模型组比较,差异无统计学意义（P＞0.05）.结论 氢气治疗可减少缺血后海马组织中NO含量及NOS活性,对海马缺血再灌注损伤起到一定的保护作用.

英文摘要：

Objective To study the effect of hydrogen on nitric oxide （NO） and its synthase in rats following acute cerebral isehemic/reperfusion （I/R） injury. Methods Seventy-two SI） rats were randomly divided into sham operation group, model group and treatment group （intraperitoneal injection with 2% hydrogen and normal saline）,24 in each group. The rats in each group were fur- ther divided into 6 h treatment group and 24 h treatment group. A middle cerebral artery occlusion model was established by Longa occlusion. Expression and activity of NOS in hippocampus tissue were detected using NOS agent kit. The NO level in hippocampus homogenate was measured by nitrate reduction. Results The number of NOS positive cells,the NO level and NOS activity were significantly higher in sham operation group than in model group 6 and 24 h after treatment （P〈 0.05） and significantly lower in treatment group than in model group 6 h after treatment （P〈 0.05） with no significant difference found between treatment group and model group （P〈0.05）. Conclusion Hydrogen protects hippocampus against I/R injury by reducing its NO level and NOS activity.