Nuglisch J, Rischke R, Krieglstein J
Institut für Pharmakologie und Toxikologie, Philipps-Universität, Marburg, BRD.
Pharmacology. 1991;42(6):333-9. doi: 10.1159/000138816.
The purpose of the present study was to investigate the influence of ischemia on postischemic metabolic activity of the brain. Furthermore, the effect of preischemic application of neuroprotective agents such as flunarizine or phencyclidine on postischemic local cerebral glucose utilization (LCGU) was examined. Forebrain ischemia in the rat was performed for 10 min with bilateral carotid clamping, administration of trimethaphan and blood withdrawal to obtain a mean arterial blood pressure of 40 mm Hg. LCGU was determined 7 days after ischemia by injecting 14C-deoxy-D-glucose in saline solution. A significant increase in LCGU in the CA1 subfield of the hippocampus was found 7 days after ischemia, whereas preischemic administration of flunarizine or phencyclidine inhibited this increase. Alterations in LCGU of other brain regions were insignificant.
本研究的目的是调查局部缺血对脑缺血后代谢活性的影响。此外，还研究了缺血前应用神经保护剂（如氟桂利嗪或苯环利定）对缺血后局部脑葡萄糖利用（LCGU）的影响。通过双侧颈动脉夹闭、静脉注射咪噻芬和放血使大鼠平均动脉血压维持在40 mmHg，造成大鼠前脑缺血10分钟。缺血7天后，通过向盐溶液中注射14C-脱氧-D-葡萄糖来测定LCGU。缺血7天后，海马CA1亚区的LCGU显著增加，而缺血前给予氟桂利嗪或苯环利定可抑制这种增加。其他脑区的LCGU变化不明显。
