脑梗死患者血浆组织型纤溶酶原激活物和抑制物活性的变化及意义

为了探讨动脉硬化性脑梗死患者急性期和恢复期的组织型纤溶酶原激活物及其抑制物活性的变化及其意义,采用发色底物法检测9例脑梗死患者和40例健康老年人的血浆组织型纤溶酶原激活物和抑制物1活性.对脑梗死患者的梗死体积和神经功能缺损进行了计算和评分,结果发现,脑梗死组急性期和恢复期的组织型纤溶酶原激活物活性分别为0.26±0.14和0.21±0.11 kIU/L,显著低于健康组(P<0.01);纤溶酶原激活物抑制物1活性分别为0.90±0.25和0.98±0.12 kAU/L,显著高于健康组(P<0.01);脑梗死体积为8.75±1.21 cm3;急性期神经功能缺损评分为18.56±3.62;组织型纤溶酶原激活物活性与脑梗死体积和神经功能缺损程度负相关(r=-0.5133,JP<0.05;r=-0.4914,P<0.05),纤溶酶原激活物抑制物1活性与脑梗死体积和神经功能缺损程度正相关(r=0.5621,P<0.05;r=0.5342,P<0.05)。结果提示,脑梗死患者急性和恢复期血浆纤溶活性显著降低,提示组织型纤溶酶原激活物与抑制物1在动脉硬化性脑梗死的病理过程中发挥了重要的作用。

The Plasmatic Activity Changes of Tissue-type Plasminogen Activator and Type 1 Plasminogen Activator Inhibitor in Patients with Arteriosclerotic Cerebral Infarction and Its Clinical Significance

Aim To explore the dynamic changes of the plasmatic activities of tPA and PAI-1 and its clinical significance by observing the plasmatic activity of tPA and PAI-1 in acute and recovery phases of the patients with arteriosclerotic cerebral infarction (ACI). Methods The plasmatic activities of tPA and PAI-1 were determined by Chromgenic Substrate methods in 91 patients with ACI and 40 normal old ages as control, while the infarction volume and the neurological damage score in those with ACI were measured. Results The plasmatic activities of tPA in acute and recovery periods of the patients with ACI was 0.26±0.14and0.21±0.11 kIU/L respectively and was significantly lower than those of the control subjects ( P< 0.01), and the plasmatic activities of PAI-1 in acute and recovery periods of the patients with ACI were 0.90 ± 0.25 and 0.98 ± 0.12 kAU/ L respectively and were significantly higher than those of the control subjects ( P< 0.01), while the infarction volume and the neurological damage score in those with ACI were 8.75 ± 1.21 cm and 18.56 ± 3.62 respectively, and the plasmatic activity of tPA was negatively related to the infarction volume and the neurological damage score in those with ACI (r = - 0.5133, P< 0. 05 and r = - 0.4914, P< 0.05 respectively ), and the plasmatic activity of PAI-1 was positively related to the infarction volume and the neurological damage score in those with ACI(r = 0.5621, p< 0.05 and r = 0.5342, p< 0.05 respectively). Conclusions The fibrinolysis activities of the acute and recovery periods of the patients with ACI decline significantly, which suggests that tPA and PAI-1 play an important role in the pathological process of arteriosclerotic cerebral infarction.