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.

基本信息

批准号：
17390392
负责人：
SAITO Nobuhito
金额：
$ 10.64万
依托单位：
The University of Tokyo (2006-2007)Gunma University (2005)
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
起止时间：
2005 至 2007
项目状态：
已结题

项目摘要

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.

迄今为止，尚未有与人类梗死相关的lacunar梗塞模型。在这项研究中，我们的目的是由于原位颈内动脉，前脉络膜动脉（ACHA）闭塞的原位穿孔动脉闭塞，开发出术语脑大脑中的lacunar中风的新模型。重量为19-42千克的墨西哥无毛微型猪进行了闭塞，使用永久性MCA闭塞方法动物的修饰可以恢复24小时，2天，1周，4周，其他天。本协议在成功生产内胶囊的成功生产中提供了91.4％的速度。对于MMEP结果，在ACHA闭塞的前6-15分钟之间暴露于缺血的内胶囊组织被认为是阴茎区域。 lacunar梗塞动物组通常在中风发作后显示出神经缺陷的迹象。尽管某种程度的运动不足仍有待来差异，但在缺血后12天，神经缺陷自发恢复到与对照动物几乎相同。另一方面，组织病理学研究表明，内部胶囊的病变逐渐扩展，这尤其归因于缺血性病变在缺血后的第一周显着扩张（p <0.05）。超微结构分析从白质缺血的扩张机理方面揭示了特征。在侵入区域，轴突最初肿胀并伴有水肿形成。最后，由于轴突中的Ca2+过载，轴突损坏了。该链反应可能会进一步提高暴露轴突诱导感性病变的膨胀的脆弱性。小血管在缺血前后，即使在慢性期，内部胶囊的量也保持不变。这可能归因于细胞敏感性的差异。

项目成果

期刊论文数量（0）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

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：
0
作者：
Honda F;Imai H;Ishikawa M;Kubota C;Shimizu T;Fukunaga M;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：
0
作者：
F Honda;H Imai;M Ishikawa;CKubota;T Shimizu;M Fukunaga;N Saito.
通讯作者：
N Saito.

Expression of Cyclophilin C-associated protein in focal cerebral ischemia in the rat

亲环蛋白C相关蛋白在大鼠局灶性脑缺血中的表达

DOI：
发表时间：
2007
期刊：
影响因子：
0
作者：
Yamaguchi R;Imai H;Hosaka M;Takeuchi T;Yoshimoto Y;Saito N.
通讯作者：
Saito N.

Focal Cerebral ischemia increases type2 iodothyronine deiodinase.

局灶性脑缺血会增加 2 型碘甲状腺原氨酸脱碘酶。

DOI：
发表时间：
2005
期刊：
J Cereb Blood Flow Metab. 25
影响因子：
0
作者：
K Seki;H Imai;T Shimizu;K Tsunekawa;T Kasahara;T Ogiwara;N Saito;M Murakami.
通讯作者：
M Murakami.

A new model of focal cerebral ischemia in the miniature pig