大鼠创伤性脑损伤早期脑组织NO含量和NOS活性的变化  

The changes of NO content and NOS activity in cerebral tissue during early tramatric brain injury in rats

作　　者：姜德华[1] 金南革[2] 刘洁[3] 杜长军[4] 

机构地区：[1]东南大学医学院附属徐州医院神经外科,徐州221009 [2]延边大学医学院生理学教研室 [3]东南大学医学院附属徐州医院检验科,徐州221009 [4]东南大学医学院附属徐州医院急诊科,徐州221009

出　　处：《江苏医药》2006年第7期640-641,共2页Jiangsu Medical Journal

摘　　要：目的探讨一氧化氮(NO)和神经元型NO合酶(nNOS)是否参与创伤性脑损伤(TBI)的发病机理。方法采用落体法大鼠TBI动物模型,观察大鼠TBI早期脑组织NO含量、NOS活性的动态变化和特异性nNOS抑制剂7-硝基吲唑(7-NI)对其的影响。结果大鼠TBI后30min脑组织NO含量和NOS活性显著升高,伤后2h两者回落,但仍高于对照组;伤后6h两者接近对照组;伤后12h NO含量仍接近对照组,而NOS活性再次高于对照组。结论NO和nNOS在创伤性脑损伤机制中可能起重要作用。Objective To investigate whether nitric oxide（NO） and neuronal NO synthase （NOS） were involved in the pathogenesis of traumatic brain injury（TBI）. Methods Using rat model of focal severe cortical contusions according to Feeney, NO content and NOS activity in ipsilateral cortex,and the effect of nNOS inhibitor 7-nitroindazole（7-NI） on them were observed. Results NO content and NOS activity in ipsilateral cortex showed a sharp increase at 30 min after TBI, and then decreased at 2 h after TBI, but remained to be higher than those in control group. At 6h after TBI, the values of NO and NOS returned to the levels of control group,but NOS activity was increased again at 12 h after TBI. Pretreatmented with 7-NI significantly inhibited NO content and NOS activity at 30 rain after TBI. Conclusion NO and nNOS may play an important role in pathophysiology of TBI.

关 键 词：创伤性脑损伤 一氧化氮 一氧化氮合酶 7-硝基吲唑 

分 类 号：R651.15[医药卫生—外科学] R995[医药卫生—临床医学]