期刊文献+

一氧化氮代谢对缺血缺氧脑组织丙二醛的影响 被引量:1

Effects of L-Arginine on Cerebral Malodialdehyde in Brain With Ischemia and Hypoxia
下载PDF
导出
摘要 目的 :探讨一氧化氮 (nitricoxide ,NO)代谢对缺血缺氧脑影响的机制。方法 :在鼠缺血缺氧之前应用NO底物左旋精氨酸 (L arginine,L Arg)和NO合酶抑制剂N 硝基 L精氨酸甲酯 (L nitro argininemethylester,L NAME) ,分别应用硝酸还原酶法和硫代巴比妥酸法测定缺血缺氧后及给药后的NO和丙二醛 (malodialdehyde,MDA)的水平。结果 :给L NAME组与缺血缺氧组比较 ,脑组织MDA水平增加 ,脑水肿明显 ;而给L Arg组的结果相反。结论 :NO代谢对缺血缺氧脑有影响作用 ,L Arg对缺血缺氧脑有保护作用。 Objective: This study was to study the effect of metabolism of nitric oxide (NO) on brain with ischemia and hypoxia. Methods: We used NO substract and inhibitor of NO synthetases L-nitro-arginine methylester (L-NAME). Before ischemia and hypoxia occurred in rats' brains, we used nitric acid reductase method and thiobarbituric acid method to measure the levels of NO and malodialdehyde (MDA) after ischemia and hypoxia group as well as after using drugs. Results: Compared with ischemia and hypoxia group, L-NAME group had increased MDA level and obvious edema in brain. However, the results in L-Arg group was the opposite. Conclusion: The metabolism of NO has effect on ischemia and hypoxia. The L-Arg had protective effect on ischemia and hypoxia.
出处 《中国医科大学学报》 CAS CSCD 北大核心 2002年第3期168-169,共2页 Journal of China Medical University
关键词 一氧化氮代谢 缺血缺氧 脑组织 丙二醛 左旗帜精氨酸 脑缺血 L-arginine malodialdehyde nitrio oxide ischemia brain
  • 相关文献

参考文献1

共引文献6

同被引文献17

  • 1Rosenbaum P, Paneth N, Leviton A, et al. A report: the definition and classification of cerebral palsy April 2006 [ J ]. Dev Med Child Neurol Suppl, 2007,109 ( 1 ) : 8-11.
  • 2Mclntosh TK. Novel pharmacologic therapies in the treatment of xperi- mental traumatic brain injury: a review [ J ]. J Neurotrauma, 1993,10 (3) :215-226.
  • 3Plangger C. Effect of gammahydroxybutyrate on intracranial pressure, mean systemic arterial pressure and cerebral perfusion pressure in ex- periment ally induced brain edema of the rat[J]. Zentralbl Neurochir,1990,51(1) :24-33.
  • 4McCloskey DP, Hintz TM, Scharfman HE. Modulation of vascular en- dothelial growth factor (VEGF) expression in motor neurons and its electrophysiological effects [ J ]. Brain Res Bull, 2008,76 ( 1-2 ) : 36- 44.
  • 5Gibson ME, Han BH, Choi J, et al. BAX contributes to apoptotic-like death following neonatal hypoxia-ischemia: evidence for distinct apop- tosis pathways [ J ]. Molecular Medicine,2001,7 (9) : 644-655.
  • 6Bain JM, Moore L, Ren Z, et al. Vascular endothelial growth factors A and C are induced in the SVZ following neonatal hypoxia-ischemia and exert different effects on neonatal glial progenitors [ J ]. Transl Stroke Res,2013,4(2) :158-170.
  • 7Zheng XR, Zhang SS, Yin F, et al. Neuroprotection of VEGF-expres- sion neural stem cells in neonatal cerebral palsy rats [ J]. Behavioural Brain Research ,2012,230 ( 1 ) : 108-115.
  • 8Oosthuyse B, Moons L, Storkebaum E, et al. Deletion of the hypoxia- response element in the vascular endothelial growth factor promoter causes motor neuron degeneration[ J]. Nat Genet, 2001,28( 2 ) : 131- 138.
  • 9Bearden SE, Segal SS. Microvessels promote motor nerve survival and regeneration through local VEGF release following ectopic reattachment [ J], Microcirculation ,2004,11 ( 8 ) :633-644.
  • 10Shiote M, Nagano I, Ilieva H, et al. Reduction of a vascular endothe- lial growth factor receptor, fetal liver kirtase-1, by antisense oligonu- cle0fides induces motor neuron death in rat spinal cord exposed to hy- poxia [ J ]. Neuroscience, 2005,132 ( 1 ) : 175-182.

引证文献1

二级引证文献2

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