Mies G, Paschen W, Hossmann K A
Department of Experimental Neurology, Max-Planck-Institute for Neurological Research, Cologne, F.R.G.
J Cereb Blood Flow Metab. 1990 Sep;10(5):638-45. doi: 10.1038/jcbfm.1990.116.
Coupling between local perfusion and metabolism was examined in Mongolian gerbils during the development of delayed neuronal death using a combination of double-tracer autoradiography and imaging of local energy state. Animals were anesthetized with 1.5% halothane and forebrain ischemia was produced by occluding both common carotid arteries. After 5 min of ischemia, brains were recirculated for 6 h and 1, 2, or 4 days. At the end of the experiment, regional cerebral blood flow (CBF) and glucose utilization (CMRglc) were determined in identical brain section with [131I]iodoantipyrine and [14C]deoxyglucose, respectively. Adjacent sections were taken for imaging of ATP and glucose using substrate-specific bioluminescence reactions. In the CA1 subfield of control animals, CBF and CMRglc amounted to 81 +/- 8 ml 100 g-1min-1 and 69 +/- 2 mumol 100 g-1min-1, respectively, and the calculated CBF/CMRglc ratio was 1.18 +/- 0.12 ml/mumol (mean +/- SD). After ischemia, the CBF/CMRglc ratio increased to 1.31 +/- 0.14, 1.43 +/- 0.16, 1.45 +/- 0.16, and 1.56 +/- 0.18 ml/mumol following 6 h and 1, 2, or 4 days recirculation, respectively. Glucose levels did not change during the 6 h to 4 day recirculation period in the hippocampal CA1 subfield. In the same region, ATP levels were unchanged during 6 h to 2 day postischemic recovery but reduced to about 70% after 4 days of recirculation. The results indicate that a mismatch of the flow--metabolism couple following transient ischemia does not appear to contribute to the postischemic maturation of delayed neuronal death in selectively vulnerable brain regions.
在蒙古沙鼠延迟性神经元死亡发展过程中，采用双示踪剂放射自显影和局部能量状态成像相结合的方法，研究了局部灌注与代谢之间的耦合关系。动物用1.5%氟烷麻醉，通过阻断双侧颈总动脉造成前脑缺血。缺血5分钟后，大脑再灌注6小时以及1、2或4天。实验结束时，分别用[131I]碘安替比林和[14C]脱氧葡萄糖在相同脑切片中测定局部脑血流量（CBF）和葡萄糖利用率（CMRglc）。取相邻切片，利用底物特异性生物发光反应对ATP和葡萄糖进行成像。在对照动物的CA1亚区，CBF和CMRglc分别为81±8 ml·100 g-1·min-1和69±2 μmol·100 g-1·min-1，计算得到的CBF/CMRglc比值为1.18±0.12 ml/μmol（平均值±标准差）。缺血后，再灌注6小时以及1、2或4天后，CBF/CMRglc比值分别增至1.31±0.14、1.43±0.16、1.45±0.16和1.56±0.18 ml/μmol。在海马CA1亚区，葡萄糖水平在再灌注6小时至4天期间没有变化。在同一区域，缺血后恢复6小时至2天期间ATP水平未变，但再灌注4天后降至约70%。结果表明，短暂缺血后血流-代谢耦合的不匹配似乎并未促成选择性易损脑区延迟性神经元死亡的缺血后成熟。
