The effects of cerebral ischemia on the rat choroid plexus
The effects of cerebral ischemia on the rat choroid plexus
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DOI：
10.1038/sj.jcbfm.9600224
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发表时间：
2006-05-01
影响因子：
6.3
通讯作者：
Keep, Richard F.
中科院分区：
文献类型：
--
作者：
Ennis, Steven R.;Keep, Richard F.
虽然脑缺血的血脑屏障效应已被广泛研究，但很少关注缺血诱导的脉络丛损伤，形成血-脑脊液（CSF）屏障（BSCFB）。本研究观察了三种缺血模型大鼠侧脑室脉络丛（LVCP），双侧颈总动脉闭塞（2 VO）+低血压伴或不伴再灌注和永久性大脑中动脉（MCA）闭塞伴或不伴串联颈总动脉闭塞。使用[C-14]-N-异丙基-p-碘苯丙胺评估血流量，并通过组织水肿、[C-14]谷氨酰胺转运改变和BSCFB破坏（用[H-3]菊粉测量）评估LVCP损伤。2 VO+低血压使LVCP血流量减少87%（P < 0.01），LVCP谷氨酰胺转运进行性减少。与皮质相比，再灌注时无LVCP充血或延迟性低灌注，但有明显的BSCFB中断。2 VO+降压30 min再灌注6 h后，脑脊液中[H-3]菊糖含量增加3倍（P < 0.05）。血-CSF屏障而不是血-脑屏障破坏似乎是增强[H-3]菊粉进入海马的主要原因。大脑中动脉闭塞合并和不合并颈总动脉闭塞仅导致LVCP血流减少53%和38%，但诱导LVCP水肿。结果表明，LVCP在绝对血流量或MCA闭塞模型中诱导损伤所需的血流量减少百分比方面选择性地易受缺血性损伤。缺血后早期BCSFB的破坏可能会增强化合物从血液向靠近脑室系统的区域的运动，并参与迟发性神经元死亡。
Although the blood-brain barrier effects of cerebral ischemia have been extensively examined, less attention has focused on ischemia-induced damage to the choroid plexuses that form the blood-cerebrospinal fluid (CSF) barrier (BSCFB). This study examined the rat lateral ventricle choroid plexuses (LVCP) in three ischemic models, bilateral common carotid artery occlusion (2VO) + hypotension with or without reperfusion and permanent middle cerebral artery (MCA) occlusion with or without a tandem common carotid artery occlusion. Blood flow was assessed using [C-14]-N-isopropyl-p-iodoamphetamine, and LVCP injury by tissue edema, alterations in [C-14]glutamine transport and BSCFB disruption (measured with [H-3]inulin). 2VO + hypotension caused an 87% reduction in LVCP blood flow (P < 0.01) and a progressive reduction in LVCP glutamine transport. In contrast to cortex, there was no LVCP hyperemia or delayed hypoperfusion on reperfusion, but there was marked BSCFB disruption. After 30 mins of 2VO + hypotension with 6 h of reperfusion, the [H-3]inulin entry into CSF was increased threefold (P < 0.05). Blood-CSF barrier rather than blood-brain barrier disruption appeared to be the main cause of enhanced [H-3]inulin entry into hippocampus. Middle cerebral artery occlusion with and without a tandem common carotid artery occlusion only caused 53% and 38% reductions in LVCP blood flow but induced LVCP edema. Results suggest that the LVCP is selectively vulnerable to ischemic injury in terms of the absolute blood flows or, for the MCA occlusion models, the % reductions in flows required to induce injury. BCSFB disruption early after ischemia may enhance the movement of compounds from blood to areas close to the ventricular system and participate in delayed neuronal death.