Cerebrovascular adaptation in chronic hydrocephalus
Cerebrovascular adaptation in chronic hydrocephalus
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DOI：
10.1097/00004647-200103000-00012
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发表时间：
2001-03-01
影响因子：
6.3
通讯作者：
Gdowski, MJ
中科院分区：
文献类型：
--
作者：
Luciano, MG;Skarupa, DJ;Gdowski, MJ
这项研究描述了伴随慢性进行性脑积水的局部血管改变。15只狗接受了脑积水的手术诱导，并用于组织学研究。动物分为4组：手术对照组、短期(小于或等于5周)、中期(8周)和长期(10~12周)组。在人工识别皮质灰质、白质和尾状核的血管后，通过成像量化计算血管直径、密度和管腔面积。尾状核毛细血管内径缩小23.5%至30.2%(P<；0.01)，12周后恢复正常。12周时皮质灰质毛细血管密度较手术对照组降低53.5%(P<；0.05)，但随后增加到234.8%(P<；0.01)。尾状核内的毛细血管密度最初并没有下降；然而，远期组的毛细血管密度显著高于手术对照组(172.8%至210.5%，P<；0.01)。总体而言，管腔面积在短期内有所减少，但在较长期内有所恢复。胶质纤维酸性蛋白(GFAP)免疫组织化学染色显示，与枕叶皮质相比，尾状核的GFAP染色和反应星形胶质细胞不同。这一数据表明，毛细血管密度和直径的增加可能是一种适应性过程，允许在慢性脑积水的缺氧环境中维持足够的脑血流灌注和代谢支持。
This study characterizes the regional changes in vascularity, which accompanies chronic progressive hydrocephalus. Fifteen dogs underwent surgical induction of hydrocephalus and were used for histologic studies. Animals were divided into 4 groups: surgical control, short term (less than or equal to5 weeks), intermediate term ((8 weeks), and long term (10 to 12 weeks). Vessel diameter, density, and luminal area were calculated by imaging quantification after manual vessel identification in the cortical gray, white matter, and caudate nucleus. Capillary vessel diameter decreased 23.5% to 30.2% (P < 0.01) in the caudate, but then returned to normal at 12 weeks. Capillary vessel density decreased 53.5% (P < 0.05) in the cortical gray, but then increased to 234.8% (P < 0.01) over surgical controls at 12 weeks. There was no initial decrease in capillary density in the caudate; however, the long-term group capillary density was significantly greater (172.8% to 210.5%, P < 0.01) than surgical controls. Overall, there was a short-term decrease in lumen area, with recovery in the longer term. Glial Fibrillary acidic protein (GFAP) immunohistochemistry demonstrated the pattern of GFAP staining and reactive astrocytes differed in the caudate compared with the occipital cortex. This data suggest that an increase in capillary density and diameter may be an adaptive process allowing maintenance of adequate cerebral perfusion and metabolic support in the hypoxic environment of chronic hydrocephalus.