The role of Platelet-activating factor (PAF) in cerebral vasospasm after subarachnoid hemorrhage

脑脊液中血小板活化因子(PAF)水平在SAH发病后逐渐升高，随后下降。脑血管痉挛脑梗死组SAH后5~9d PAF浓度明显高于非脑梗死组。相反，PAF乙酰水解酶活性在SAH后逐渐降低，然后升高。脑梗死组同期酶活性低于非梗死组。用琼脂糖凝胶过滤(J Neurosurg 80：31-36,1994)可检测到两个抑制PAF乙酰水解酶活性的峰，即空泡体积和13kD。E5880还能减轻基底动脉的收缩。此外，E5880组出现缺血性改变的频率低于对照组。E5880可降低兔血浆血栓素B_2浓度。静脉注射E5880是预防血管痉挛发生的一种很有前途的方法(J NeuroSurg In Press)。

Levels of platelet-activating factor (PAF) in CSF showed gradual increase after the onset of SAH,with a subsequent decrease. The PAF concentration between 5 and 9 days after SAH was greater in patients with cerebral infarction due to vasospasm than in patients without infarction. Conversely, PAFacetylhydrolase activity decreased gradually after SAH,then increased. The enzyme activity for the same period was smaller in patients with cerebral infarction than in patients without infarction. Two peaks of inhibitory activity against PAFacetylhydrolase, void volume and 13kD,were detected on SephacrylS-200HR gel filtration (J Neurosurg 80 : 31-36,1994).Neurological deterioration was largely prevented in the rabbits which received a PAF antagonist, E5880. Basilar artery constriction also was reduced by E5880. Furthermore, E5880 group demonstrated ischemic changes less frequently than the controls. Plasma thromboxane B_2 concentrations were reduced in rabbits treated with E5880. The intravenous administration of E5880 is a promising approach preventing the occurrence of vasospasm (J Neurosurg in press).