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Studies on the white matter damage after ischemia of perforating brain artery.

Studies on the white matter damage after ischemia of perforating brain artery.
脑动脉穿支缺血后脑白质损伤的研究.
批准号:
17390392
负责人:
SAITO Nobuhito
金额:
$10.64万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2005
资助国家:
日本
项目状态:
已结题
起止时间:
2005 至 2007

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中文摘要
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英文摘要
There has been no previous animal model of lacunar infarction relevant to the lacunar infarction of human so far. In this study, we aimed to develop a new model of lacunar stroke in gyrencephalic brain as a result of in situ small perforating arterial occlusion of internal carotid artery, anterior choroidal artery (AchA) occlusion. Mexican hairless miniature pigs, weighing 19-42 kg, were undergone to AchA occlusion, using a modification of the permanent MCA occlusion method Animals were allowed to recover for 24 hours, 2 days, 1 week, 4 weeks and other days. The present protocol provided a 91.4% rate in successful production of the internal capsule. For MMEP results, internal capsule tissues that were exposed to ischemia between the first 6 - 15 minutes of AchA occlusion were considered penumbra zone. Lacunar infarction animal group usually displayed signs of neurological deficit after stroke onset. Although some degree of motor deficit remains to be unrecovered, the neurological deficit spontaneously recovered to became nearly same as to the control animals at 12 day after ischemia. On the other hand, histopathological study revealed that the lesion of internal capsule expands gradually as time dependent manner which is particularly attributed to significant expansion of the ischemic lesion during the first week after ischemia (P<0.05). Ultrastructural analysis unveiled the characteristics in terms of the mechanism of expansion in white matter ischemia. At peri-infarct zone the axon was initially swollen accompanied with the edema formation. Finally the axon was ireversiblly damaged presumably due to the Ca2+ overload in axons. This chain reaction might further increase the vulnarability of the exposed axon to induce the expansion of the ishemic lesion. The small vessels amount at internal capsule remains constant before and after ischemia, even in the chronic phase. This is probably attributed to the difference in cellular susceptibility.
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Cilostazol Attenuates Both Gray and White Matter Damage in a Rodent Model of Focal Cerebral Ischemia.
西洛他唑可减轻局灶性脑缺血啮齿动物模型中的灰质和白质损伤。
DOI: --
发表时间: 2006
期刊: Stroke 37
影响因子: --
作者: [F Honda, H Imai, M Ishikawa, CKubota, T Shimizu, M Fukunaga, N Saito.]
通讯作者: N Saito.
DOI: 10.1016/j.neures.2005.08.002
发表时间: 2005-11-01
期刊: NEUROSCIENCE RESEARCH
影响因子: 2.9
作者: [Tomizawa, S, Imai, H, Saito, N]
通讯作者: Saito, N
Cilostazol attenuates both gray and white matter damage in a rodent model of focal cerebral ischemia
西洛他唑可减轻局灶性脑缺血啮齿动物模型中的灰质和白质损伤
DOI: --
发表时间: 2006
期刊: Stroke 37
影响因子: --
作者: [Honda F, Imai H, Ishikawa M, Kubota C, Shimizu T, Fukunaga M, Saito N.]
通讯作者: Saito N.
DOI: 10.2176/nmc.46.111
发表时间: 2006-03
期刊: Neurologia medico-chirurgica
影响因子: 1.9
作者: [Tatsuya Shimizu;Ken-ichi Sugawara;M. Tosaka;Hideaki Imai;K. Hoya;T. Takeuchi;Tomio Sasaki;N. Saito]
通讯作者: Tatsuya Shimizu;Ken-ichi Sugawara;M. Tosaka;Hideaki Imai;K. Hoya;T. Takeuchi;Tomio Sasaki;N. Saito
16
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    • 项目类别:
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    • 资助金额:
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      2013
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      23659683
    • 项目类别:
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    • 资助金额:
      $2.58万
    • 财政年份:
      2011
    • 负责人:
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    • 批准号:
      20249063
    • 项目类别:
      Grant-in-Aid for Scientific Research (A)
    • 资助金额:
      $30.78万
    • 财政年份:
      2008
    • 负责人:
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    • 依托单位:
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    • 批准号:
      13470283
    • 项目类别:
      Grant-in-Aid for Scientific Research (B)
    • 资助金额:
      $7.87万
    • 财政年份:
      2001
    • 负责人:
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