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脳卒中易発症高血圧ラット（SHR-SP）を用い，脳虚血後再灌流時の脳水分含量，局所脳血流量（LCBF）に及ぼす細胞膜Cl−透過性抑制剤ONO−1016の影響について検討した。SHR-SPを対照（偽手術のみ）群，非治療（saline投与）群，およびONO−1016（100μg／kg／minを虚血前より投与）群に分けた。脳虚血は，麻酔／人工呼吸下に両側頸動脈結紮にて1時間行い，その後再灌流させ2時間後に断頭し，脳水分含量（乾燥重量法）およびLCBF（［14C］‐iodoantipyrine法）を測定した。その結果，対照群に比べ虚血後再灌流時には終脳と間脳一中脳領域の一部で脳水分含量の増加とLCBFの減少が起きたが，ONO−1016群では非治療群に比べ，水分含量は中隔，線条体および中脳で低値となり，またLCBFは線条体および海馬で高値となった。以上のことから，ONO−1016は一過性脳虚血後の脳浮腫および低灌流発現を軽減する作用を有することが分かった。
The effects of ONO-1016, as an inhibitor of Cl-/ HCO3- exchange, on the brain edema and circula-tory failure following cerebral ischemia were examined in stroke-prone spontaneously hyperten-sive rats (SHR-SP) . SHR-SP were divided intothree groups : control (sham-operation) , non-treat-ed, ONO-1016 group, respectively. Cerebral is-chemia was produced by bilateral carotid artery occlusion (BCAO) for 1 hr and then following reper-fusion. The brain water content and local cerebral blood flow (LCBF) were determined by dry-wet method and 14C-iodoantipyrine method 2 hr after start of reperfusion. ONO - 1016 was given intravenously at a dose of 100 μg/kg/min prior to ischemia.
The brain water content increased in septum (SP) , amygdala (AM) in both non-treated and ONO -1016 groups compared from those in control group. However, brain water contents in SP and midbrain were lower in ONO-1016 group than those in non-treated group. LCBFs decreased to 50-80% in SP, cerebral cortex (CT), striatum (ST), hippocampus (HC) and AM in non-treated group, while LCBFs decreased to 60-80% in SP, CT, ST, AM in ONO-1016 group when compared from those in control group. Decrease of LCBF in ST and HC in ONO-1016 group were less severe than those in non-treat-ed group.
From these results, ONO-1016 may prevent the brain edema formation associated with hypoper-fusion during reperfusion period after ischemia in SHR-SP.
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