腦缺血變化於水腦症之影響: 腦缺血變化增生因子, VEGF及PLGF於實驗性水腦症之分析及其重要性
Date Issued
2004-12-31
Date
2004-12-31
Author(s)
杜永光
DOI
922314B002254
Abstract
Background and Purpose— In chronic hydrocephalus, a role for tissue hypoxia
resulting from cerebrovascular compression is suggested. The purpose of this study
was to evaluate the geographic and temporal pattern of angiogenic factor elevation
after adult kaolin-induced hydrocephalus.
Methods— In 22 adult Sprague-Dawley rats, kaolin hydrocephalus was induced and
quantitative reverse transcription polymerase chain reaction (QPCR) was performed
at 1 week (short term) and 4 weeks (long term). Immunostaining of vascular
endothelial growth factor receptor 1 (Flt-1) was also performed at 1 (short term), and
4 (long term) weeks.
Results— At 1 weeks, Placenta growth factor (PlGF) and Flt-1 was increased in
Striatal area and hippocampus but not cortical areas. Four weeks after hydrocephalus
induction, PlGF elevation persisted but Flt-1 elevation goes down. At 4 weeks, Flt-1
immunohistochemical changes in the periventricular area became most evident.
Conclusions— The observed Flt-1 and PlGF elevation supported the hypothesis that
ischemia is the major mechnism of hydrocephalic damage. The proinflammatory
cytokine PlGF may have significant role in the pathogenesis of chronic
hydrocephalus.
Publisher
臺北市：國立臺灣大學醫學院外科
Type
report
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