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。由于血管痉挛而发生脑梗死的患者在SAH后5 - 9天的PAF浓度高于无梗死的患者。相反，PAFacetylhydrolase活性在SAH后逐渐降低，然后升高。同一时期脑梗死患者的酶活性低于无梗死患者。用SephacrylS-200HR凝胶过滤法检测了PAFacetylhydrolase的两个抑制峰，空穴体积和13kD (journal of neurojournal)（中国神经外科杂志，80:31-36,1994）。在接受PAF拮抗剂E5880的家兔中，神经退化在很大程度上得到了预防。E5880也能减少基底动脉的收缩。此外，与对照组相比，E5880组出现缺血性改变的频率更低。E5880可降低家兔血浆血栓素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 neurosurgery 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).