ARACHIDONATE TRANSPORT THROUGH THE BLOOD-RETINA AND BLOOD-BRAIN-BARRIER OF THE RAT AFTER REPERFUSION OF VARYING DURATION FOLLOWING COMPLETECEREBRAL-ISCHEMIA

The permeability-surface area product (PS) of [1-C-14]arachidonate at the blood-retina and blood-brain barrier was determined by short carot id perfusion in young Wistar rats 1 or 6 h after recovery period follo wing complete cerebral ischemia induced by temporary cardiac arrest. F or the retina and structures of visual system, hypothalamus and olfact ory bulb there was no significant difference over sham-operated rats a mong mean PSs. For cortex, hippocampus and striatum, significant incre ases were found at both time intervals of recovery after cardiac arres t. The ischemia-reperfusion model was characterized by a significant i ncrease in tissue conjugated diene in the hippocampus and microsomal l ysophosphatidylcholine acyltransferase activity in the cortex. Consist ent with these findings, we also show ultrastructural evidence mainly represented by partial opening of interendothelial junctions and mild signs of tissue edema in surrounding neuropil, suggesting barrier leak iness predominantly in the cortex, hippocampus and striatum but almost absent in the retina microvessels. Our results indicate that ischemia -reperfusion does affect influx through blood-brain barrier into regio nal structures of rat central nervous system of arachidonate, a metabo lic substrate and lipid mediator rapidly incorporated into microcapill ary and brain lipids. The data also suggested that: (i) reactive oxyra dicals were moderately generated during the early phase of ischemic-re perfusion process in the rat, (ii) after reperfusion, in vitro suscept ibility of different brain regions to iron-induced peroxidation was hi ghest in the hippocampus and lowest in the cortex and striatum; (iii) membrane phospholipid repair mechanisms were activated at the same tim e. (C) 1998 ISDN. Published by Elsevier Science Ltd.