The effects of cerebral ischemia on the rat choroid plexus.

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 [(14)C]-N-isopropyl-p-iodoamphetamine, and LVCP injury by tissue edema, alterations in [(14)C]glutamine transport and BSCFB disruption (measured with [(3)H]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 [(3)H]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 [(3)H]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.