摘要
目的 研究一氧化氮 (NO)在脊髓缺血再灌注损伤中的作用。方法 夹闭大鼠腹主动脉制成缺血再灌注模型 ,随机分成L -NAME组和再灌注组 ,L -NAME组每日腹腔注射一氧化氮合酶(NOS)非特异性抑制剂L -硝基精氨酸甲酯 (L -NAME) 10mg/kg体重 ,两周时取大鼠脊髓做NOS免疫组织化学染色、组织学及超微病理观察。结果 脊髓缺血再灌注后前角运动神经元出现固有型一氧化氮合酶 (cNOS)阳性表达 ,同时伴随前角运动神经元损伤 ;应用L -NAME后可减少cNOS的异常表达 ,减轻前角运动神经元损伤。结论 局部组织中NO产生增多可能是脊髓再灌注损伤的机制之一。
Objective To clarify the effect of nitrous oxide(NO) for the treatment of spinal cord ischemia reperfusion injury. Methods The animal modle was established by clamping rats abodominal aorta. The animals were randomly divided into NG-nitiro-L-arginine methylester (L-NAME) group and reperfusion group; the animals in L-NAME group received intraperitoneal injection of L-NAME at a dose of 10 mg/kg body weight everyday. Two weeks after experiment rat spinal cord was sectioned and stained by nitrous oxide synthase(NOS) immunochemistry and the ultrastructural histopathologic changes were observed. Results Expression of constitutive NO synthase(cNOS) was induced in spinal ventral horn motorneuron with motorneuron damage after spinal cord ischemia reperfusion, animals that were given L-NAME had lower expression of cNOS and less damage of motorneuron. Conclusion Increase of NO production in local tissue may cause reperfusion injury.
出处
《中华骨科杂志》
CAS
CSCD
北大核心
2000年第2期111-113,共3页
Chinese Journal of Orthopaedics
