This experiment was conducted to study the change of the activity of NOS and the content of NO, and the influence of Xuesaitong and L-NNA on the change in Striatal Hemorrhage rabbits, and to investigate the mechanism of action of NO on the cerebral hemorrhage and the protective effect of those two pharmaceuticals on the cerebullar neurons. Fifty-six healthy Ha-erbin white rabbits, 4 moon's old, were divided into the model group, control group of sham operation and the treatment group of striatal hemorrhage rabbits with Xuesaitong and L-NNA injection in random. The mode of cerebral hemorrhage rabbits were established in this surgery , we determined the activity of NOS and the content of NO in different time after striatal hemorrhage in hemorrhagic corpus striatum by biochemical technology. The results indicated that the activity of NOS increased at 6 hours after striatal hemorrhage, and increased to the highest at 3 days, and then decreased gradually from 3 to 9 days, and basically returned to normal levels at 9 days. The activity of NOS in the two therapy groups were lower than that in model grope at every time extremely notable difference or notable difference (P<0. 01 or P<0. 05), and the level of decreasing the activity of NOS in the group of L-NNA was lower than that in the group of Xuesaitong between 6 hours to 1 day (P<0. 05). The change of the content of NO and the activity of the NOS was accordant primitively and direct correlation. SABC immunohistochemical method was used to detected the neuronal NOS positive neurons in each corpus striatum. We found that the density of striatal neuronal NOS positive neurons increased, cell coloring became saturate, soma-sectional area and the length of longest tuber became smaller. The density of neuron reduced, and the soma-sectional area and the length of longest tuber ameliorated significantly after treatment (P<0. 05). The results suggested that NO work in the process of cerebral hemorrhage damage, and the high concentrations of No play a neurotoxicity role in damage to brain tissue. Xuesaitong and L-NNA reduce the content of NO in the corpus striatum by inhibiting the activity of NOS, which has a significant protective effect on neurons in cerebral hemorrhage rabbits.%为了研究家兔脑纹状体出血后一氧化氮合酶(NOS)活性和一氧化氮(NO)含量的变化及L-NNA和血塞通对其变化的影响,探讨NO在脑出血损伤中的作用机制及2种药物对脑神经元的保护作用.选取4月龄健康哈白兔56只,随机分为假手术对照组、模型组,脑纹状体出血血塞通治疗组及脑纹状体出血L-NNA治疗组,手术建立家兔脑出血模型,应用生化检测技术测定各组脑纹状体出血后不同时间出血侧纹状体NOS活性及NO含量.结果表明,模型组脑纹状体内NOS活性6h开始升高,3d达到高峰,随后逐渐下降,9d时基本恢复至正常水平；2治疗组纹状体NOS活性在各时间点极显著或显著低于模型组(P＜0.01或P＜0.05),并且L-NNA在6h～1d时降低脑纹状体NOS活性的程度好于血塞通治疗组(P＜0.05)；NO含量的变化与NOS活性的变化基本一致,二者成正相关；利用SABC免疫组织化学法方法检测各组脑纹状体神经型NOS(nNOS)阳性神经元,发现模型组纹状体nNOS阳性神经元密度增加,细胞着色加深,胞体截面积和最长突起长度变小,经过治疗后神经元密度降低,胞体截面积和最长突起长度显著改善(P＜0.05).结果提示:NO参与了脑出血损伤过程,高浓度的NO能发挥神经毒性作用损害脑组织；血塞通和L-NNA通过抑制NOS的活性,降低了脑纹状体NO的含量,对脑出血家兔的脑神经元具有明显的保护作用.
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