缺乏证据表明NMDA受体或多胺直接参与大鼠脑缺血后的血脑屏障损伤。

Lack of evidence for direct involvement of NMDA receptors or polyamines in blood-brain barrier injury after cerebral ischemia in rats.

作者信息

Preston E, Webster J, Palmer G C

机构信息

Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario, Canada.

出版信息

Brain Res. 1998 Nov 30;813(1):191-4. doi: 10.1016/s0006-8993(98)00981-0.

DOI:10.1016/s0006-8993(98)00981-0

PMID:9824696

Abstract

It is hypothesized that after various types of brain injury, blood-brain barrier (BBB) opening and vasogenic edema result from excessive neuronal release of glutamate and stimulation of capillary N-methyl-d-aspartate (NMDA) receptors linked to polyamine (putrescine) synthesis in endothelial cells. We produced cerebral ischemia in rats and measured BBB opening 6 h later as the increase in regional transfer constants (Ki) for blood to brain diffusion of [3H]sucrose. Such BBB opening was not mitigated by drugs which block NMDA receptors (MK801 or AR-R 15896AR) or polyamine synthesis (difluoromethylornithine). These results question generality of the capillary NMDA receptor/polyamine hypothesis.

摘要

据推测，在各种类型的脑损伤后，血脑屏障（BBB）开放和血管源性水肿是由于神经元过度释放谷氨酸，并刺激与内皮细胞中多胺（腐胺）合成相关的毛细血管N-甲基-D-天冬氨酸（NMDA）受体所致。我们在大鼠中制造了脑缺血，并在6小时后测量BBB开放情况，以[3H]蔗糖从血液到脑扩散的区域转运常数（Ki）增加作为指标。这种BBB开放并没有被阻断NMDA受体的药物（MK801或AR-R 15896AR）或多胺合成抑制剂（二氟甲基鸟氨酸）所缓解。这些结果对毛细血管NMDA受体/多胺假说的普遍性提出了质疑。