期刊文献+

兴奋性氨基酸受体拮抗剂对清醒大鼠脑缺血再灌注损伤的保护作用 被引量:3

Effects of excitatory amino acid receptor antagonists on brain ischemic reperfusion damage in rats
下载PDF
导出
摘要 目的:观察兴奋性氨基酸受体拮抗剂对清醒大鼠全脑缺血再灌注损伤的影响。方法:采用我们改进的清醒大鼠脑缺血模型,于缺血前15min、再灌注6h分别腹腔注射5mg/kg或10mg/kg的竞争性N-甲基-D天冬氨酸(NMDA)受体拮抗剂CPP、25mg/kg或50mg/kg的非竞争性NMDA受体拮抗剂氯胺酮、15mg/kg或30mg/kg的!-氨基羟甲基恶唑丙酸(AMPA)受体拮抗剂NBQX;观察其对不同脑区(脑下脚、海马CA1/2区、CA3区与CA4区、齿状回)神经细胞数目的变化以及纹状体病理损伤的影响,并监测肛温的变化。结果:各组脑缺血与再灌注期间的肛温和纹状体病理损伤无显著差异。应用CPP、氯胺酮或NBQX的大鼠多个脑区正常神经细胞数目明显多于生理盐水对照组。结论:兴奋性氨基酸受体拮抗剂CPP、氯胺酮、NBQX对缺血性脑损伤具有明显的保护作用,并且这种保护作用不是由于体温下降所致。 Objective To investigate the effect of excitatory amino acid receptor antagonists on brain ischemic reperfusion damage in rats, Methods The 4-vessel occlusion rat model of global ischemia improved by us was used in our study. Five mg/kg or 10 mg/kg CPP, 25 mg/kg or 50 mg/kg ketamine, and 15 mg/kg or 30 mg/kg NBQX were given with i.p at 15 min before ischemia and 6 h after reperfusion, respectively. The rectal temperature was also monitored. The neuronal numbers changes of subiculum, hippocampal zone CA1/2, zone CA3 and zone CA4, supra and infra lobes of dentate gyrus and the pathological changes of striatum were obersved. Results There was no significant difference of rectal temperature and no difference of the pathological changes of striatum between the diversed groups. The normal neuronal numbers of different regions among the rats who received CPP, ketamine or NBQX were more than those who received NS. Conclusion There is significant protection effect of excitatory amino acid receptor antagonists on brain ischemic reperfusion damage in rats.
出处 《实用医学杂志》 CAS 2007年第7期950-952,共3页 The Journal of Practical Medicine
关键词 再灌注损伤 兴奋性氨基酸 拮抗剂 保护 Reperfusion injury Excitatory amino acid Antagonists Protection
  • 相关文献

参考文献12

  • 1White B C,Sullivan J M,Degracia D J,et al.Brain ischemia and reperfusion:molecular mechanisms of neuronal injury[J].J Neurol Sci,2000,179(S1-2):1-33.
  • 2NIshizawa Y.Glutamate release and neuronal damage in ischemia[J].Life Sei,2001,69(4):369-381.
  • 3Harukuni I,Bhardwaj A.Mechanisms of brain injury after global cerebral ischemia[J].Neurol Clin,2006,24(1):1-21.
  • 4Pulsinelli W A,Bfiedey J B.A new model of bilateral hemispheric ischemia in the unanesthetized rat[J].Stroke,1979,10(3):267-272.
  • 5Pulsinelli W A,Brierley J B,Plum F.Temporal profile of neuronal damage in a model of transient forebrain ischemia[J].Ann Neurol,1982,11(5):491-498.
  • 6Hou X Y,Zhang G Y,Yan J Z,et al.Activation of NMDA receptors and L-type voltage-gated calcium channels mediates enhanced formation of Fyn-PSD95-NR2A complex after transient brain ischemia[J].Brain Res,2002,955(1-2):123-132.
  • 7Shen W,Zhang C,Zhang G.Nuclear factor kappaB activation is mediated by NMDA and non-NMDA receptor and L-type voltagegated Ca(2+) channel following severe global ischemia in rat hippocampus[J].Brain Res,2002,933(1):23-30.
  • 8Diemer N H,Jorgensen M B,Johansen F F,et al.Protection against ischemic hippocampal CA1 damage in the rat with a new non-NMDA antagonist,NBQX[J].Acta Neurol Scand,1992,86(1):45-49.
  • 9Nellgard B,Wieloch T.Postischemic blockade of AMPA but not NMDA receptors mitigates neuronal damage in the rat brain following transient severe cerebral ischemia[J].J Cereb Blood Flow Metab,1992,12(1):2-11.
  • 10Suzuki Y,Takagi Y,Nakamura R,et al.Ability of NMDA and nonNMDA receptor antagonists to inhibit cerebral ischemic damage in aged rats[J].Brain Res,2003,964(1):116-120.

同被引文献46

引证文献3

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