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缺血再灌注对大鼠视网膜氧自由基及形态的影响 被引量:2

Effects of ischemia/reperfusion on oxygen free radicals and morphology in rat′s retina
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摘要 目的观察缺血再灌注(RIR)过程中大鼠视网膜氧自由基(OFR)及视网膜形态的变化过程。方法采用前房灌注液体形成16kPa高眼压而建立RIR模型。检测视网膜组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性及行视网膜光学显微镜的组织学观察。结果与空白对照组相比,缺血组SOD、MDA水平分别有明显降低与升高(P<0·05);与缺血组相比,再灌注各组SOD水平继续降低(P<0·05),MDA水平继续升高(P<0·05)。缺血再灌注各组大鼠视网膜细胞丢失明显,逐渐由水肿变为萎缩损伤,较空白对照组严重。结论OFR含量在视网膜缺血再灌注过程中逐渐升高,可导致视网膜持续性病变。 Objective To study the variation of OFR and retinal morphology in rats during RIR. Methods Retinal ischemia was induced in SD rats by increasing the intraocular pressure to 16 kPa for 60 minutes via cannulation into the anterior chamber. Contents of SOD and MDA in retina were measured and retinal morphology was observed. Results The content of SOD was markedly decreased while the content of MDA was increased in ischemia group as compared with those in placebo group ( P 〈 0. 05 ). The content of SOD was further decreased while the content of MDA was further increased in reperfusion groups as compared with those in the ischemia group ( P 〈 0. 05 ). In RIR groups,loss of cell was obvious, edema gradually turnel to atrophy. Injury in RIR groups was serious than that in placebo group. Conclusion OFR is gradually increased during RIR, which causes continuous lesion in retina.
出处 《安徽医科大学学报》 CAS 北大核心 2006年第3期264-266,共3页 Acta Universitatis Medicinalis Anhui
关键词 视网膜 再灌注损伤 动物 实验 大鼠 retina reperfusion injury animals rats
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  • 1卢步峰,鲁友明,黄诒森.蛋白激酶C对大鼠缺血海马突触体谷氨酸摄取的调控作用[J].生物化学杂志,1994,10(3):371-375. 被引量:12
  • 2[1]Zhu MD, Cai FY. The effect of Salviae Milti orrhizae Co. on the retrograde axoplasmic transport in the optic nerve of rabbits with chronic IOP elevation [J]. Chin J Ophthalmol, 1991;27(3):174-178.
  • 3[2]Bonomi L, Saettone MS, Bucci G. Methods to produce ocular hyperte nsion in animals [J]. Ophthalmic Drug Deliv, 1987;11(1):107-116.
  • 4[3]Paulo DK, Alexander KB. Nitric oxide synthase inhibition delays axonal degeneration and promotes the survival of axotomized retinal ganglion cells [J ]. Exp Neurol, 1999;158(2):366-381.
  • 5[4]Vorwerk CK, Hyman BT, Miller JW, Husain D, Zurakowski D, Huang P L, Fishman MC, Dreyer EB. The role of neuronal and endothelial nitric oxide sythase in retinal excitotoxicity [J]. Invest Ophthalmol Vis Sci, 1997;38(9):2038- 2044.
  • 6[5]Hattori Y, Oka M, Kasai K. Lipopolysaccharide treatment in v ivo induces tissue expression of GTP cyclohydrolase I mRNA [J]. FEBS Lett, 1995;368(2):336-33 8.
  • 7[6]Kijlstra A. The role of cytokines in ocular inflammation [J]. Br J Ophthalmol, 1994;78(3):885-887.
  • 8[7]Babu JS, Kanangat S, Rouse BT. T cell cytokine mRNA expressio n during the course of the immunopathologic ocular disease herpetic stromal keratitis [J]. J Immunol, 1995;154(12):4822-4829.
  • 9[8]Masanori H, Kazuaki M, Kano H, Tujikawa A, Ogura Y, Honda Y, Yosbimura N. Roles of constitutive nitric oxide synthase in postischemic rat ret ina [J]. Invest Ophthalmol Vis Sci, 1999;40(2):450-458.
  • 10Lam T T,Invest Ophthalmol Vis Sci,1999年,40卷,967页

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