A study of hemostasis in ischemic cerebrovascular disease. III. Abnormalities in vascular plasminogen activators, antiactivators and alpha 2-antiplasmin.
A sample of in all 119 patients with ischemic cerebrovascular disease (TIA and minor stroke) below the age of 55 years, were submitted for testing of fibrinolysis in the late recovery phase after acute disease. Defective fibrinolysis, as tested after venous stasis, was found in patients (p less than 0.01) as compared to controls using a conventional fibrin plate method. A new chromogenic peptide substrate method showed a similar tendency. Antiactivator activity, measured as antiurokinase, using a peptide substrate, was significantly higher (p less than 0.01) in young female patients than in female controls. Alpha 2-antiplasmin (peptide substrate method) was significantly (p less than 0.001) higher in female than male patients. However, no correlation was found between inhibitors of fibrinolysis and defective fibrinolysis after venous occlusion. Furthermore, in a pilot study of vein biopsies, normal content of vascular plasminogen activators was found in the majority of cases. Thus, it is suggested that defective fibrinolysis in most cases reflects a disturbed release function.
D000293:Adolescent; D000328:Adult; D002545:Brain Ischemia / Q000097:blood*; D005260:Female; D005342:Fibrinolysis; D006487:Hemostasis; D006801:Humans; D008297:Male; D008875:Middle Aged; D010960:Plasminogen Activators / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015849:Plasminogen Inactivators; D012306:Risk; D014680:Veins / Q000378:metabolism; D000979:alpha-2-Antiplasmin / Q000378:metabolism*
D015849:Plasminogen Inactivators; D000979:alpha-2-Antiplasmin; D010960:Plasminogen Activators