The Determination Of Cerebral Infarction In Patients With Protein C System And Antithrombin System

To invc's igate the changes of protein and ant i throniH n system i r. plasma in patients with infarction an-.its clinic si gn i I'i can;Methods concentrations of protein C (PC), total protein S(PS), free proiein S(PS) and t hrombin-anti thrombi n Illcompl ex (TAT) were measured in LLISA. The activity of activated protein C(.APC) and ant i thrombi n 111 (AT-III) were measured by the chrornogenic met hod. Results T ie levels of PC and FPS were reduced significant 1y(P<0.05) in cerebral infarction patients of acute phase and convalescent phase, whi le I'AI and APC levels were increased significantly(P<0.01) than the controls. The levels of activity AT-I11 reduced significant 1y(P<0. 05) in the acute phase of cerebral infarction, but the difference was not statistically significant(P>0.05) during the recovery stage of cerebral infarction. The activity of APC was higher among conical infarction than among subcortical infarction. The severer I he patient's condition was, the higher TAT was,while the lower PC and FPS were. As compared to the patients with cerebral infarction more or than the age 50, PC and FPS were decreased significantly in patients before the age 50. FPS was reduced significantly in patients with cerebral infarction who had the history of transient ischemic attack(TIA), as compared to those who no the history of TIA. APC was positively associated with TAT and inversely correlated to AT-III. The correlation between TAT and AT-Ⅲ was actual ly riegat i ve, while TPS and FPS was negative. There no correlation between PC, FPS and the concentration of blood Conclusion There are act i vat ion of coagulation and abnormality of anticoagulant system in patients with cerebral infarction. The abnormality of anticoagulant factor played a major role in pathogenesis course of cerebral infarction. Low levels of PC and FPS in patients with cerebral infarction not only reflect the hypercoagulable state and prognosis outcome,but also may be a hereditary risk factor for young cerebral infarct.