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目的探讨自发性蛛网膜下腔出血(SAH)后血及脑脊液(CSF)中纤溶活性的变化规律及正常CSF中的纤溶状态。方法组织型纤溶酶原激活物的活性(tPA:A)及纤溶酶原抑制物的活性 (PAI:A)测定采用发色底物法,纤溶酶原抑制物-1(PAI-1)及D-二聚体(D-D)定量测定采用酶联免疫吸附试验(ELISA)双抗体夹心法,血及CSF标本在SAH后0-3 d(急性期),4-9 d(再出血高峰期),及 14-21 d(吸收期)留取三次;正常对照组留取一次。结果 SAH患者血液中,急性期tPA:A显著低于对照组,并随病程延长显著升高,至14-21 d达正常水平,与对照组差异无显著意义;急性期PAI:A 及D-D水平显著高于对照组,并随病程延长而显著降低,至14-21 d降至正常水平,与对照组差异无显著意义;各期PAI-1含量与对照组差异无显著意义。对照绀CSF中,测不到tPA:A及PAI:A及 PAI-1,D-D测得值很小,为(0．28±0．36)mg/L。 SAH患者CSF中,各期测不到tPA:A及PAI:A,但 PAI-1含量急性期显著升高并随病程延长而显著降低,D-D急性期显著升高并随病程延长而显著降低,至14-21 d 与对照组无显著性差异。结论 SAH后血中不存在纤深活性亢进。对照组CSF中不含有纤溶酶系。SAH患者CSF中纤溶活性急性期升高而后降低,于14-21 d恢复到正常水平。再出血高峰期血及CSF中反映纤溶活性的指标变化均显著低于急性期,提示再出血与血及CSF中纤溶活性无关。故SAH后不宜长期大剂量应用抗纤溶药物来预防再出血。
Objective To investigate the changes of fibrinolytic activity in blood and cerebrospinal fluid (CSF) after spontaneous subarachnoid hemorrhage (SAH) and the fibrinolytic status in normal CSF. Methods The activities of tissue plasminogen activator (tPA: A) and plasminogen activator inhibitor (PAI-A) were determined by using the chromogenic substrate method, plasminogen inhibitor-1 ) And D-dimer (DD) were determined by enzyme-linked immunosorbent assay (ELISA) double antibody sandwich method. Blood and CSF samples were collected at 0-3 d after SAH (acute phase), 4-9 d Period), and 14-21 d (absorption period) to take three times; normal control group once. Results The levels of tPA: A in acute phase of SAH patients were significantly lower than those in control group, and increased significantly with the prolongation of the course of disease. Up to the normal level in 14-21 d, there was no significant difference with the control group. The levels of PAI: A and DD in acute phase Significantly higher than the control group, and with the prolonged significantly decreased, to 14-21 d reduced to normal levels, with no significant difference between the control group; PAI-1 content in each phase and the control group no significant difference. In control CSF, tPA: A and PAI: A and PAI-1 were not detected, and D-D was very small (0.28 ± 0.36) mg / L. In patients with SAH, tPA: A and PAI: A were not detected in all stages of the disease, but PAI-1 levels were significantly increased in the acute phase and significantly decreased with the prolongation of the course. The acute phase of DD was significantly increased and decreased significantly with the prolongation of the course. Between 14-21 d and the control group no significant difference. Conclusion There is no hypertrophy in the blood after SAH. The control group did not contain plasmin in the CSF. Fibrinolytic activity in CSF increased and then decreased in SAH patients, returning to normal after 14-21 days. The indexes of fibrinolytic activity in blood and CSF at the peak of rebleeding were significantly lower than those in acute phase, suggesting that rebleeding had no relation with fibrinolytic activity in blood and CSF. Therefore, after SAH should not be long-term high-dose anti-fibrinolytic drugs to prevent rebleeding.