[Effects of the subarachnoid hemorrhage on the release of arachidonate metabolites from canine cerebral arteries].

Release of arachidonate metabolites from isolated canine cerebral arteries into perfusing medium were estimated using radioimmunoassay (RIA) in vitro. The cerebral arteries were isolated from dogs sustained experimental subarachnoid hemorrhages (SAH) and the results were compared with that of normal canine cerebral arteries. The amount of 6-Keto-PG F1 alpha (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), PGF2 alpha, PGD2 were also measured, but release of these arachidonate metabolites were little compared with PGI2 or PGE2. The amount of 6-Keto-PGF1 alpha and PGE2 released from the cerebral 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-PGF1 alpha 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 involved in the pathogenesis of cerebral vasospasm. The release of PGs from canine pial arteries induced 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 arachidonate was increased.