Prostacyclin and vasospasm in subarachnoid hemorrhage from ruptured intracranial aneurysm. A preliminary clinical study.
Experimental and clinical observations suggest the importance of arachidonate metabolites in the genesis of symptomatic cerebral vasospasm after subarachnoid hemorrhage. Prostacyclin (PG12) has a well demonstrated vasodilator action. The authors monitored CSF prostacyclin concentration in 12 consecutive cases of subarachnoid hemorrhage with the purpose of correlating the prostacyclin concentration trend with the clinical course and the risk for vasospasm. In three cases patients presented with clinical and radiological signs of vasospasm. CSF prostacyclin concentration showed a typical decreasing trend, which amounted to a minor form of protection from vasospastic agents. The nine cases which did not develop vasospasm demonstrated no significant changes in the prostacyclin CSF concentration trend. The authors also presented four cases in which cisternal CSF samples were available. In one case of developing vasospasm, the cisternal prostacyclin concentration was seven times lower than the highest lumbar CSF concentration. In three cases without evidence of vasospasm cisternal CSF demonstrated a balanced biochemical situation and a minor risk of vasospasm.
D015121:6-Ketoprostaglandin F1 alpha / Q000134:cerebrospinal fluid; D000293:Adolescent; D000328:Adult; D000368:Aged; D011464:Epoprostenol / Q000134:cerebrospinal fluid*; D005260:Female; D006801:Humans; D002532:Intracranial Aneurysm / Q000150:complications*; D002546:Ischemic Attack, Transient / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D013345:Subarachnoid Hemorrhage / Q000134:cerebrospinal fluid* / Q000150:complications / Q000209:etiology
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol