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氯胺酮对全脑缺血大鼠的脑保护作用 被引量:6

The neuroprotection of ketamine in a model of transient forebrain cerebral ischemia rats
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摘要 目的探讨氯胺酮对全脑缺血大鼠的脑保护作用。方法健康成年SD大鼠30只,随机均分为缺血加氯胺酮组(A组)、缺血组(B组)、假手术组(C组)。以Pulsinelli-Brierley方法为标准建立四动脉阻断法全脑缺血模型,A、B组行全脑缺血15min后再灌注,其中A组于全脑缺血5min时腹腔给氯胺酮100mg/kg,B组相同时间腹腔内注射同体积生理盐水,C组分离椎动脉及颈总动脉后不行全脑缺血。再灌注3d后经心脏灌注固定后取脑制作石蜡切片,分别行HE染色观察海马CA1区神经元存活数目和TUNEL法检测海马CA1区神经元凋亡。结果C组大鼠海马CA1区神经元大部分存活,少量神经元凋亡;B组神经元很少存活,大量凋亡,细胞计数明显少于C组(P<0.01);A组神经元存活数目明显少于C组,但多于B组(P<0.01),凋亡数目明显多于C组,但少于B组(P<0.01)。结论氯胺酮对脑缺血大鼠具有一定的脑保护作用。 Objective To investigate the neuroprotection of ketamine in a model of cerebral ischemia rats. Methods Thirty adult healthy SD rats were randomly divided into three groups with 10 rats each. The global cerebral ischemia model was produced by four-vessel occlusion for 15 min as described by Pusinelli-Brierley in group A and B. The rats in group C were not suffered from forebrain cerebral ischemia after bilateral vertebral arteries and common carotid arteries seperated. The rats of group A were injected with ketamine 100 mg/kg into peritoneal cavity 5 min after cerebral ischemia,while the rats of group B were treated with the same volume physiologic saline at the same time. The survived neurons in the CA1 sector of the hippocampus were observed with histopathological technique, meanwhile the neurones apoptosis in the CA1 sector hippocampus was detected by TUNEL method 3 days after cerebral reperfusion. Results There were a lot of neurons survived and a few TUNEL-positive cells observed in group C. Meanwhile the survived neurons were more and TUNEL-positive cells were less in group A than those in group B (P〈0.01). But the survived neurons were less and TUNEL-positive cells were more in group A than those in group C (P〈0.01). Conclusion Ketamine has a certain neuroprotective effect on ischemic rats.
出处 《临床麻醉学杂志》 CAS CSCD 2008年第8期683-685,共3页 Journal of Clinical Anesthesiology
基金 青岛市科技局立项课题(编号:2005kzd-22)
关键词 氯胺酮 缺血-再灌注损伤 脑保护 Ketamine Ischemia-reperfusion injury Neuroprotection
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参考文献10

  • 1张研,马正良,曾因明.NMDA受体介导的缺血性脑损伤机制的研究进展[J].国外医学(麻醉学与复苏分册),2004,25(5):285-288. 被引量:8
  • 2Pulsinelli WA,Brierley JB,Plum F. Temporal profile of neuronal damage in a model of transient forebrain ischemia. Ann Neurol, 1982,11: 491-498.
  • 3Nicholls D, Attwell D. The release and uptake of excitatory amino acids. Trends Pharmacol Sci, 1990,11:462-468.
  • 4Simon RP,Swan JH,Griffiths T,et al. Blockade of N-mthyl- D-aspartate receptors may protect against ischemic damage in the brain. Science, 1984,226 : 850-852.
  • 5Wieloch T. Hypoglycemia-induced neuronal damage prevented by an N methyl D-aspartate antagonist. Science, 1985, 230:681-683.
  • 6Orser BA,Pennefather PS, MacDonald JF. Multiple mechanisms of ketamine blockade of N-methyl-D-aspartate recep tors. Anesthesiology, 1997,86:903-917.
  • 7Pei L, Li Y, Zhang GY, et al. Mechanisms of regulation of tyrosine phosphorvlation of NMDA receptor subunit 2B after cerebral ischemia/ reperfusion. Acta Pharmacol Sin, 2000, 21:695-700.
  • 8张轩萍,梁月琴,汤允昭.地西泮对大鼠脑缺血再灌注损伤的保护作用[J].中国新药与临床杂志,1998,17(4):209-211. 被引量:2
  • 9梅元武,胡波,邱小鹰,孙圣刚.地西泮对大鼠脑缺血再灌注损伤皮质内氨基酸含量的影响[J].卒中与神经疾病,2001,8(3):147-149. 被引量:7
  • 10Zausinger S, Hungerhuber E, Baethmann A, et al. Neurologi cal impairment in rats after transient middle cerebral artery occlusion:a comparative study under various treatment para digms. Brain Res, 2000,863:94-105.

二级参考文献38

  • 1[1]Shuib A, Kanthan R. Amplification of inhibitoyr mechanisms in cerebral ischemia: an alternative approach to neuronal protection. Histolistopathol, 1997,12(1): 185
  • 2[2]Zivin JA, Girolami U, Kochhar A, et al. A modelfor quantitative evaluation of embolic stroke therapy, Brain res, 1987,435: 305
  • 3[3]Hall ED, Andrus PK, Fleck TJ, et al. Neuroprotective properties of benzodapine recptor, partial agonist PNU-101017 in the gerbril forebrain ischemia model. B J Cereb Blood Flow Metab, 1997, 17 (8):875
  • 4[4]Inglefield JR, Wilson CA, Schwarta-Bloom RD. Effect of transient cerebral ischemia on gamma-aminobutyric acid A receptor alpha 1subunit-immunoreactive interneurons in the gerbril CA1 hippocapus. Hippocampus, 1997,7(5):511
  • 5[5]Schwartz-Bloom RD, Mcdonough KJ, Chase PJ, et al. Long-tem neuroprotectionn by benzodapine: full versus partial agnonists after transient cerebral ischemia in the gerbil. J cereb Blood Flow Metab,1998,1815: 548
  • 6[6]Kleckner NW,Dingledine R. Requirment for glycine in activation of NMDA-receptors expressed in xenopus oocytes. Science, 1988,241:835
  • 7[7]John JW, Ascher P. Glycine potentiates the response in cultureed mouse brain neurons. Nature, 1987,325: 529
  • 8[8]Regan MH,Song D, Vander Heide S J, et al. Free radicals and the ischemia-evoked extracellular accumulation of anino acids in rat cerebral cortex. Neurochem Res, 1997,22 (3): 273
  • 9Bertolino M, Vicini S, Mazzetta J, et al. Phencyclidine and glycine modulate NMDA-activated high conductance cationic channels by acting at different sites. Neurosci Lett, 1988,84(3) :351-355.
  • 10Patel J, Zinkand WC, Thomposn C, et al. Role of glycine in the N-methyl-Daspastate-mediated neuronal cytotoxicity. J Neurochem, 1990, 54 (3): 849-854.

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