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去骨瓣减压术对大鼠局灶性脑缺血细胞凋亡的影响 被引量:3

Effect of Decompressive Craniectomy on Changes of Apoptosis after Focal Cerebral Ischemia in Rats
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摘要 目的:探讨去骨瓣减压术对局灶性脑缺血细胞凋亡的影响。方法:改良Koizumi法制作脑缺血动物模型,6 h后在缺血侧行去骨瓣减压术,采用 TUNEL法测定减压术后4、8、16、24 h皮质和纹状体区细胞凋亡变化,并采用流式细胞仪测定术后4和 24 h细胞凋亡的改变。结果:在术后第24小时,去骨瓣减压组皮质区凋亡细胞比例与对照组相比显著减少(P<0.05和P<0.01),而两组纹状体区凋亡细胞比例在各时间点均无显著性差异(均P>0.05)。结论:皮质区细胞凋亡的减少可能是去骨瓣减压术对局灶性脑缺血保护作用的重要机制之一。 Aim:To investigate the effect of decompressive craniectomy on the changes of apoptosis after focal cerebral ischemia.Methods: Focal cerebral ischemia was induced by using an endovascular occlusion technique. Decompressive craniectomy was performed at insult side 6 h after ischemia. The proportion of apoptotic cells in TUNEL staining in both cortex and striatum was calculated at 4,8,16,24 h after decompression. And the percentage of apoptotic cells was directly detected with flow cytometry at 4 and 24 h after the decompressive procedure.Results:Comparing with non-decompressive group, the percentage of apoptotic cells in the cortex of the decompressive group was found to be decreased significandy at 24 h (P < 0.05 and P < 0.01). No significant difference was found in the striatum with the both methods ( P > 0.05). Conclusion: Decompressive craniectomy could prevent apoptosis in the ischemic cortex 24 h after operation, which was responsible for the fact that decompressive craniectomy could alleviated ischemic damage.
出处 《中国临床神经科学》 2003年第1期37-41,共5页 Chinese Journal of Clinical Neurosciences
关键词 脑缺血 去骨瓣减压术 细胞凋亡 治疗 cerebral ischemia decompressive craniectomy apoptosis
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参考文献10

  • 1Doerfler A, Forsting M, Reith W, et al. Decompressive craniectomy in a rat modd of maligrant cerebral hemispheric stroke: experimental support for an aggressive therapeutic approach[J]. J Neurosurg, 1996,85:853-859
  • 2刘正言,周良辅,黄峰平,毛颖.去骨瓣减压术对大鼠局灶性脑缺血保护作用的有效时间窗[J].中国临床神经科学,2001,9(2):162-165. 被引量:10
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二级参考文献12

  • 1[9]Doerfler A, Forsting M, Reith W, et al. Decompressive craniectomy in a ratmodel of malignant cerebral hemispheric stroke: experimental support for anaggressive therapeutic approach. J Neurosurg, 1996; 85: 853-859
  • 2[10]Valtysson J, Jiang M, Persson L. Transient elevation of the intracranialpressure increases the infarct size and perifocal edema after subsequentmiddle cerebral artery occlusion in the rat. Neurosurgery, 1992;30:887-890
  • 3[11]Engelhom T, Doerfler A, Kastrup A, et al. Decompressive craniectomy,reperfusion, or a combination for early treatment of acute "malignant”cerebral hemispheric stroke in rats? Potential mechanisms studied by MRI.Stroke, 1999; 30:1456-1463
  • 4[12]Hatashita S, Hoff JT. The effect of craniectomy on the biomechanics ofnormal brain. J Neurosurg, 1987 ;67:573-578.
  • 5[1]Krieger DW, Demchuk AM, Kasner SE, et al. Early clinical andradiological predictors of fatal brain swelling in ischemic stroke. Stroke,1999; 30: 287-292
  • 6[2]Rieke K, Schwab S, Krieger D, et al. Decompressive surgery in space-occupying hemispheric infarction: result of an open prospective trial. CritCare Med, 1995 ;23:1576-1587
  • 7[3]Kalia KK, Yonas H. An aggressive approach to massive middle cerebralartery infarction. Arch Neurol, 1993; 50:1293-1297
  • 8[4]Cater BS, Ogilvy CS, Candia GJ, et al. One-year outcome afterdecompressive surgery for massive nondominant hemispheric infarction.Neurosurgery, 1997;50:1168-1176
  • 9[5]Longa EZ, Weinstein PR, Carison S, et al. Reversible middle cerebralartery occlusion without craniectomy in rats. Stroke, 1989;20:84-91
  • 10[6]Menzies SA, Hoff JT, Betz LA. Middle cerebral artery occlusion in rat.s:aneurological and pathological evaluation of a reproducible model.Neurosurgery, 1992; 32:100-107

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