Rapid increase of prostaglandin F2-alpha in neurons after subarachnoid hemorrhage in rats: an immunohistochemical study

Publisher Website
Google Scholar
Abstract
The effects of subarachnoid hemorrhage (SAH) with various degrees of increase in intracranial pressure (ICP) on the staining of prostaglandin F2-alpha (PG F2α) were studied in rat brains. SAH was produced in 18 rats by injection of 0.18–0.20 ml of autologous arterial blood/100 g body weight into the cisterna magna. By changing the speed of injection, the ICP was transiently increased by 346±68 (mean±S.D.) mm Hg in eight rats (including three pretreated with indomethacin), by 200±42 mm Hg in five rats, and by 6±4 mm Hg in the other five. Three rats injected with the same volume of mock cerebrospinal fluid (CSF) with ICP increased by 217±67 mm Hg and five normal rats without injection served as controls. All animals were decapitated 15 min after injection. The cryosections were stained for PG F2α using an indirect immunofluorescence method. Positive staining for PG F2α was noted only in pial vessels in all normal and mock-CSF-injected rats. In SAH rats with ICP increased by 6±4 mm Hg, there was a positive reaction in hippocampal neurons and Purkinje cells as well as blood vessels. SAH rats with higher ICP showed stronger PG F2α staining in the above areas, as well as in cerebellar granule cells. All rats pretreated with indomethacin showed a smaller increase in staining. The above results indicate that subarachnoid blood clots per se produce a rapid increase of PG F2α in neurons and blood vessels of both cerebrum and cerebellum, and that this increase is augmented by intracranial hypertension.