Neovascularization with blood-brain barrier breakdown in delayed neuronal death.
Neovascularization with blood-brain barrier breakdown in delayed neuronal death.
复制标题
新血管形成与血脑屏障破坏导致延迟性神经元死亡。
DOI：
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Y. Watanabe
中科院分区：
文献类型：
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作者：
Y. Kataoka;Y. Cui;H. Yamada;K. Utsunomiya;H. Niiya;H. Yanase;Y. Nakamura;A. Mitani;K. Kataoka;Y. Watanabe
中枢神经系统的各种急性病理事件，如缺血、出血和创伤，常常引起脑水肿。水肿可能会持续数天或数周，同时引起神经功能的广泛损伤，无论原始损伤的程度如何，并且通常导致死亡。迟发性水肿被认为是血管源性的;然而，水肿诱导的潜在机制仍然未知。我们发现沙鼠海马CA 1区及其周围的血管细胞增殖延迟，血脑屏障破坏，该区域在短暂缺血后2-6天参与延迟性凋亡性神经元死亡。通过（3）H-胸苷掺入评估的血管细胞增殖在缺血后4-6天最为显著，同时观察到外源性染料或内源性血清白蛋白从血管外渗。我们提出迟发性神经元死亡中的新生血管形成是神经事件后脑水肿进展的一个原因。
Various kinds of acute pathological events in the central nervous system, such as ischemia, hemorrhage, and trauma, often cause brain edema. The edema may advance for days or weeks while inducing extensive damage in neural function, regardless of the extent of the original damage, and often results in death. Delayed edema is thought to be vasogenic; however, the mechanism underlying edema induction remains unknown. We found delayed vascular cell proliferation with a blood-brain barrier breakdown in and around the gerbil CA1 hippocampus, a region known to be involved in delayed apoptotic neuronal death 2-6 days after transient ischemia. Vascular cell proliferation, assessed by (3)H-thymidine incorporation, was most prominent 4-6 days after ischemia, and extravasation of exogenously applied dye or endogenous serum albumin from blood vessels was observed concomitantly. We propose neovascularization in delayed neuronal death as a cause of brain edema advancing days after neurological events.
局灶性脑缺血中静脉注射碱性成纤维细胞生长因子减少梗塞的时间窗。
影响因子：
5
作者：
Ren,JM;Finklestein,SP
通讯作者：
Finklestein,SP
影响因子：
4.8
作者：
Provias, J;Claffey, K;Guha, A
通讯作者：
Guha, A