Prostaglandin D2 monitoring in human CSF after subarachnoid hemorrhage: the possible role of prostaglandin D2 in the genesis of cerebral vasospasm

Experimental and clinical studies indicate that cerebral vasospasm following subarachnoid hemorrhage (SAH) may be caused by changed biochemical properties of the endothelium and vascular smooth muscle cell exposed to vasoactive substances synthetized by cerebral arteries and released in clotted blood. Many compounds have been identified in CSF from SAH patients: Thromboxanes A₂ and B₂, Prostaglandins F_2α, E₂ and D₂ are the major prostanoids incriminated in the causation of cerebral arterial spasm. We have monitored the CSF PGD₂ concentrations with serial lumbar punctures at different intervals from the hemorrhage in 16 patients admitted for SAH: PGD₂ was measured with radioimmunoassay as its 9-methoxy derivative. The lumbar CSF PGD₂ concentration ranges from 0,11 to 1.53 ng/ml. In 7 cases vasospasm was angiographically demonstrated. 9 patients presented no clinical or radiological evidence of vasospasm. In 5 cases cisternal CSF samples were available at the operation by cisternal punctures. There was no correlation between CSF PGD₂ concentration and clinical course. In the 7 cases with evidence of vasospasm a significant increase of CSF PGD₂ corresponded to neurological deterioration. In all 9 cases without evidence of vasospasm CSF PGD₂ concentration trend was in a steady-state. The cisternal CSF PGD₂ concentration was higher than lumbar CSF concentration in cases with arterial spasm. This suggests the importance of the clotting phenomenon in vasospasm onset after SAH. PGD₂ is one of the most important spasmogens in clotted blood. Although its role in the genesis of vasospasm onset remains to be defined, its vasospatic action, in addition to that of other analogous compounds, seems to be relevant.