6-ketoprostaglandin-f1-alpha and Brain-Damage--Chronic

CSF eicosanoid levels are raised following subarachnoid haemorrhage but not sufficiently to be vasoactive per se within the cerebral circulation. Rebleeding and intraventricular haemorrhage are two factors associated with a worse outcome after aneurysmal SAH. We have examined the effects of these two factors on the CSF levels of TXB2 (TXA2 metabolite), PG6-keto F1 alpha (prostacyclin metabolite), PGF2 alpha and PGE2 in 44 patients following subarachnoid haemorrhage. In 15 patients who had received no non-steroidal anti-inflammatory agent or dexamethasone, intraventricular haemorrhage increased the median levels of all four eicosanoids in ventricular CSF by 2.1-5.1-fold. In 4 patients who rebled, the CSF median levels of all four eicosanoids were raised up to 250-fold over the normal range. These concentrations are just sufficient to have cerebrovascular and neuromodulatory effects.

Topics: 6-Ketoprostaglandin F1 alpha; Aspirin; Brain Damage, Chronic; Cerebral Ventricles; Dexamethasone; Dinoprost; Dinoprostone; Drug Therapy, Combination; Eicosanoids; Humans; Infusions, Intravenous; Intracranial Aneurysm; Nimodipine; Prognosis; Recurrence; Reference Values; Subarachnoid Hemorrhage; Thromboxane B2