脳表動脈よりreleaseされるアラキドン酸代謝物とクモ膜下出血による変化

EFFECTS OF THE SUBARACHNOID HEMORRHAGE ON THE RELEASE OF ARACHIDONATE METABOLITES FROM CANINE CEREBRAL ARTERIES

　抄録　赤血球溶血液（hemolysate）は，脳動脈を収縮させ，また脳動脈からprostaglandin （PG）様物質をreleaseさせる。そこで，正常犬とクモ膜下出血犬の脳表動脈からreleaseされるPGsをradioilnmuno-assay （RIA）法を用いて比較定量し，またこれらの血管にhemolysateを作用させる事により，どのような種類のPGsがreleaseされるかを検討した。正常脳表動脈からは，主としてPGI₂とPGE₂がreleaseされ，量的には，PGI₂がPGE₂の約4倍releaseされた（PGl₂ 455±84（n＝7），PGE₂ 177±72（n＝8）ng／g dry weight／min）。これに対してクモ膜下出血後の脳表動脈では，PGF₂αが僅かに増加した以外は，すべてのPGsが減少し，特にPGI₂は有意に減少した（110±34（n＝6） ng／g dry weight／min）。また，hemolysate作用による増減は，正常犬，クモ膜下出血犬脳表動脈いずれも有意の増減を認めなかった。クモ膜下出血による脳表動脈よりのPGI₂ releaseの減少により，収縮性PGが優位となる事が，脳血管攣縮の一役を担っていると考えられる。hemolysate作用で脳動脈からreleaseされるPG様物質は，PGD₂，PGE₂, PGF₂α，　PGI₂, thromboxane A₂以外の物質であると考えられる。

Release of arachidonate metabolites from iso-lated canine cerebral arteries into perfusing medium were estimated using radioimmunoassay (RIA) in vitro. The cerebral arteries were isolated from dogs sustained experimental subarachnoid hemor-rhages (SAH) and the results were compared with that of normal canine cerebral arteries. The a-mount of 6-Keto-PG Fia(stable metabolite of PGI₂) and PGE₂ released from normal cerebral arteries were 455±84(n=7) and 177±72(n=8) ng/min/g dry weight (mean±SEM), respectively. Among other arachidonate metabolites, TXB₂ (stable metabolite of TXA₂), PGF₂α, PGD₂ were also measured, but release of these arachidonate metabolites were lit-tle compared with PGI₂ or PGE₂. The amount of 6-Keto-PGF₁α and PGE₂ released from the cere-bral arteries subjected to subarachnoid hemorrhage were 110±34(n=6), 169±40(n=6) ng/min/g dry weight respectively. In SAH group, release of 6-Keto-PGF₁α had diminished remarkably, but no remarkable quantitative change were seen among other arachidonate metabolite between normal and SAH groups. The diminution of PGI₂ release in the cerebral artery subjected to SAH may be in-volved in the pathogenesis of cerebral vasospasm. The release of PGs from canine pial arteries in-duced by the exposure of the pial arteries to red blood cell hemolysate was also estimated by RIA. The release of PGE₂ tended to increase following to exposure to hemolysate but no other arachido-nate was increased.