脑梗死患者血浆炎症因子、纤溶活性的变化及对神经功能的影响

The fluctuation of plasma inflammation cytokines,fibrinolytic activity in patients with acute cerebral in farction and effect on nerve function

目的通过观察急性脑梗死患者血浆中的Ⅷ因子相关抗原(vWF)、P-选择素(P-Selectin)、白细胞介素-6(IL-6)、组织型纤溶酶原激活物(t-PA)及快速抑制物(PAI-1)的变化规律,探讨炎症因子及纤溶活性在脑梗死发生、发展、转归过程中的作用。方法采用酶联免疫吸附(ELISA)及发色底物法对40例急性脑梗死患者发病后6,12,24及72h血浆vWF,P-selectin,IL-6,t-PA及PAI-1活性进行动态测查。并与32例自愿者健康对照组进行比较。结果在急性脑梗死患者发病24h内,vWF(147.4±26.2)μg/ml、P-selectin(21±4)ng/ml、IL-6(114.5±1.5)μg/ml、PAI-1(0.79±0.24)au/ml活性明显增高,t-PA活性(0.24±0.15)iu/ml明显降低,与对照组比较差异有显著性意义(P<0.05);随时间推移vWF(118.6±24.4)μg/ml、P-selectin(14±3)ng/ml、IL-6(108.7±4.4)μg/ml、PAI-1(0.56±0.20)au/ml活性有所降低,而t-PA活性(0.43±0.11)iu/ml升高,但与正常对照组相比仍有差异(P<0.05)。结论(1)急性脑梗死患者早期存在内皮细胞损伤;(2)炎症因子参与脑部缺血性损害;(3)纤溶活性下降,说明t-PA及PAI-1参与了血栓形成的病理过程。

Aim To observe the regularity of fluctuation of plasma vWF,P-selectin,IL-6,t-PA and PAI -1act ivity in patients with acute cerebra l in-farction,and to probe their roles in the development and prognosis of cerebral infarction.Methods vWF,P-selectin,IL-6,t-PA and PAI-1activities were dynamically determined by ELISA and corresponding development substra te at the 6th,12th,24th and 72nd hour afte r the onset of acute cerebral infarction in40patients,26males and 14females,with the mean age of(65±10)years,and 32normal controls,21males and 11females,matched for sex,age and body indices.Results In the acute cerebral infarction gro up,the levels of Vwf (147.4±26.2)μg /ml,P-selectin P-selectin(21±4)ng /ml ,IL-6(114.5±1.5)μg /ml ,and PAI-1activities(0.79±0.24)aμ/ml were significantly higher ,and the l evel of t-PA activity(0.24±0.15)iμ/ml was significantly lower within the f irst 24hours,with a significant dif fer-ence from those of the control group(P<0.05);then the levels of vWF(118.6±24.4)μg /ml,P-selectin(14±3)ng /ml,IL-6(108.7±4.4)μg /ml and PAI-1activities(0.56±0.20)aμ/ml gradually decreased and t-PA increased(0.43±0.11)iμ/ml ,but with a difference form that of th e control group(P<0.05).Conclusion(1)Endothelial cell damage is ob-served in patients with acute cerebr al infarction;(2)Inflammation cytokines exacerbate brain ischemia injury;(3)The plasma fibrinolytic activity signifi-cantly lower suggests that the plasm a t-PA and PAI-1play a role in thepathogenetic progress of cerebral t hrombosis.