Beck T, Wree A, Schleicher A
Institut für Pharmakologie und Toxikologie, Philipps-Universität, Marburg, F.R.G.
Brain Res. 1990 Feb 26;510(1):74-83. doi: 10.1016/0006-8993(90)90729-u.
The influence on hippocampal glucose utilization was determined in male Wistar rats 7 days after a 10-min forebrain ischemia. Ischemia was induced by clamping of the carotid arteries and lowering blood pressure to 40 mm Hg. Despite severe neuronal damage as assessed by histological techniques, local cerebral glucose utilization (LCGU) was significantly increased in the pyramidal and radiatum layer of the CA1 sector, while in layers of the CA2, CA3 and CA4 sector and dentate gyrus. LCGU was reduced compared to non-ischemic controls. The increases in LCGU are suggested to reflect long-lasting hyperexcitation in the selectively vulnerable CA1 sector, implicating a correlation between cellular hypermetabolism and neuronal damage.
在雄性Wistar大鼠经历10分钟的前脑缺血7天后，测定其对海马葡萄糖利用的影响。通过夹闭颈动脉并将血压降至40毫米汞柱来诱导缺血。尽管通过组织学技术评估显示存在严重的神经元损伤，但CA1区锥体层和辐射层的局部脑葡萄糖利用（LCGU）显著增加，而CA2、CA3和CA4区以及齿状回的层中，LCGU与非缺血对照组相比降低。LCGU的增加被认为反映了选择性易损CA1区的持久过度兴奋，这意味着细胞高代谢与神经元损伤之间存在关联。
