期刊文献+

大鼠脑出血后一氧化氮合酶阳性神经元数目的时程变化及果糖二磷酸钠镁干预作用 被引量:1

Timed number of nitric oxide synthase-positive cells in brain of rats with intracerebral hemorrhage and influence of sodium magnesium fructose diphosphate
下载PDF
导出
摘要 目的 :研究脑出血后一氧化氮合酶 (NOS)阳性神经元的时程变化 ,以及果糖二磷酸钠镁 (FDPM )的干预作用。方法 :以胶原酶诱导法制备大鼠脑出血模型 ,应用NADPH黄递酶组织化学方法 ,观察脑出血后NOS阳性神经元随时间的变化过程 ,并观察FDPM对其影响。结果 :脑出血后NOS阳性神经元2h时明显增多 ,6h有轻度下降 ,12h再度增多 ,2 4~ 72h达高峰 ,7d (16 8h)下降 ,但仍明显高于正常。脑出血后使用 4 0 0mg·kg-1FDPM可显著减少NOS阳性神经元 ,其作用优于相似剂量的 1,6 二磷酸果糖 (FDP)和硫酸镁 ,而 133mg·kg-1的FDPM没有明显作用。结论 :脑出血后NOS活性变化呈双峰现象 ; AIM: To study the timed number of nitric oxide synthase (NOS) positive cells and the effects of sodium magnesium fructose diphophate (FDPM). METHODS: Rat model of intracerebral hemorrhage (ICH) was induced by collagenase, the timed number of NOS positive cells and the effects of FDPM on it was determined by NADPH histochemical staining. RESULTS: After the onset of ICH, the number of NOS positive cells increased obviously at 2 hours, decreased lightly at 6 hours, increased again at 12 hours, peaked during from 24 hours to 3 days, and decreased again at 7 days, but was till higher than that of normal condition. Application of FDPM decreased significantly the number of NOS positive cells after ICH, and the effect of FDPM was superior to that of fructose 1,6 diphophate or magnesium sulfate. CONCLUSION: The change of NOS activity shows two peaks after ICH, and inhibition of NOS activity may be one of the important protective mechanisms of FDPM from ICH.
出处 《中国临床药理学与治疗学》 CAS CSCD 2004年第1期80-82,共3页 Chinese Journal of Clinical Pharmacology and Therapeutics
关键词 脑出血 一氧化氮合酶 果糖二磷酸钠镁 1 6-二磷酸果糖 硫酸镁 intracerebral hemorrhage nitric oxide synthase sodium magnesium fructose diphophate fructose-1,6-diphophate magnesium sulfate
  • 相关文献

参考文献5

二级参考文献9

共引文献25

同被引文献13

  • 1刘韶华,吴颢昕,姜亚军,周红.大鼠脑出血早期脑组织神经元型一氧化氮合酶mRNA表达及中药抵当汤干预对其的影响[J].临床神经病学杂志,2005,18(6):436-439. 被引量:3
  • 2Zhang Q,Jia LS.The mechanism of secondary lesion after spinal cord injury[J].Zhongguo Changshang Zazhi,2003,19 (4):249-251.
  • 3Ladecola C,Xu X,Zhang F,et al.Marked induction of calcium-independent nitric oxide synthase artivity after focal cerebral ischemia[J].J Cereb Blood Flow Metab,1995,15(1):52-59.
  • 4Laufs U,Eldres M.Neuroprotection mediated by changes in the endothelial actin cytoskeletonLJ].J Clin Invest,2000,106 (1):15-24.
  • 5Raines K W,Cao G L,Porsuphatana S.Nitric oxide inhibition of ERK1/2 activity in ceils expressing neuronal nitric-oxide synthase[J].J Biol Chem.2004,279(6):3933-3940.
  • 6Leker R R,Teichner A,Ovadia H.Expression of endothelial nitric oxide synthase in the ischemic penumbra relationship to expression of nuronal nitric oxide synthase and vascular endothelial growth factor[J].Brain Research,2001,90(9):1-7.
  • 7O'Neill M J.Murray T K,Mc Carty D R.ARL 17477,a selective nitric oxide synthase inhibitor,with neuroprotective efects in animal models of g obal and focal cerebral ischaemia[J].Brain Research,2000,871 (2):234-244.
  • 8Brown G C,Borutaite V.Nitric Oxide Inhibition of M itochon-drial Respiration and its Role in Cell Death[J].Free Radic Biol Med(S0891-5849),2002,33(11):1440-1450.
  • 9庞刚,肖泉,钟书,唐秀文,曾敬初,叶劲,刘若平,蓝胜勇.一氧化氮对脑出血病人预后的影响[J].广西医学,2007,29(8):1144-1146. 被引量:1
  • 10陈红霞,刘远新,贾红娥.便秘对脑出血病人内皮素和一氧化氮及病情的影响[J].中西医结合心脑血管病杂志,2007,5(9):889-890. 被引量:14

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部