Cerebral hypoxia and embolism evoke the release of prostaglandin (PG)-like substances, predominantly of E type, into cerebral venous blood. This has been shown by bioassay used for monitoring the level of PG-like substances in sagittal sinus blood (ssb) in dogs. Hypoxia was induced by inhalation of 8% O2 in N2, embolism by an injection of air into internal carotid artery. This led to an increase in the level of PG-like substances in ssb, with no detectable change in the concentration of PGs in peripheral venous blood, indicating that PGs detected in ssb originate from cerebral venous outflow. The output amounted 6 ng/ml (in PGE2 equivalents). Hydrocortisone (HC) in a dose of 30 mg/kg suppressed the release of PG-like substances induced by either hypoxia or embolism. These results were confirmed by radioimmunoassay of PGs in ssb. Plasma levels of PGs E and F2 alpha were elevated following cerebral embolism as compared to initial values and greatly suppressed by HC administration. Suppression of PG formation by HC in this experimental system seems to be related to the membrane--stabilizing action of this hormone. This is of interest in view of the usefulness of steroid therapy in cerebrovascular pathology.