Moroz L A, Gilmore N J
Blood. 1976 Oct;48(4):531-45.
Fibrinolytic activity of normal plasma and blood has been measured by 125l-fibrin solid phase assay. Activity of plasma is not affected by removal of plasminogenplasmin by affinity chromatography. Activities of euglobulin and pseudoglobulin fractions are approximately equal. epsilon-aminocaproic acid (EACA) (10 mM), tranexamic acid (10 mM), diisopropylfluorophosphate (DFP, 50 mM), and soybean and lima bean trypsin inhibitors (100 mug/ml) do not inhibit plasma activity at concentrations that inhibit pure plasmin and urokinase-activated plasma. Activity is not affected by glass contact and is not inhibited by inhibitors of contact or enzymatic activation of Hageman factor (hexadimethrine bromide, 100 mug/ml; cytochrome C, 250 mug/ml; spermidine, 2 mM; phenylmethylsulfonylfluoride, 1 mM). It is inhibited partially (30%-40%) by heating (56 degrees C, 30 min) and by zymosan (2.5 mg/ml; 40%-90% inhibition), and is increased by hydrazine (20 mM), salicylaldoxime (20 mM), DFP (50 mM), and tosyl-L-arginine methyl ester (TAMe, 10 mM)-the latter two at concentrations known to inhibit Cls of the classic, and factor D of the alternate complement pathways. Increase fibrinolytic activity with TAMe is associated with reciprocal decrease in classic and alternate complement pathway activity. It is concluded that normal plasma fibrinolytic activity is relatively independent of plasmin as the ultimate fibrinolytic enzyme, that Hageman factor-dependent pathways are of minor importance, and that significant heat-stable and heat-labile nonplasmin fibrinolytic activities are operative. These may include proteinases involved in complement activation, and in common control of classic and alternate complement pathways, as well as other nonplasmin proteinases.
已通过¹²⁵I-纤维蛋白固相分析法测定了正常血浆和血液的纤溶活性。通过亲和层析去除纤溶酶原-纤溶酶后，血浆活性不受影响。优球蛋白和假球蛋白组分的活性大致相等。ε-氨基己酸（EACA，10 mM）、氨甲环酸（10 mM）、二异丙基氟磷酸（DFP，50 mM）以及大豆和利马豆胰蛋白酶抑制剂（100 μg/ml）在抑制纯纤溶酶和尿激酶激活血浆的浓度下，并不抑制血浆活性。活性不受玻璃接触的影响，也不受接触激活或Hageman因子酶促激活抑制剂（溴化己二甲铵，100 μg/ml；细胞色素C，250 μg/ml；亚精胺，2 mM；苯甲基磺酰氟，1 mM）的抑制。加热（56℃，30分钟）和酵母聚糖（2.5 mg/ml；40%-90%抑制）可使其部分抑制（30%-40%），而肼（20 mM）、水杨醛肟（20 mM）、DFP（50 mM）和甲苯磺酰-L-精氨酸甲酯（TAMe，10 mM）可使其增加——后两者在已知抑制经典途径的C1s和替代补体途径的D因子的浓度下。TAMe增加纤溶活性与经典和替代补体途径活性的相应降低相关。结论是，正常血浆纤溶活性相对独立于作为最终纤溶酶的纤溶酶，Hageman因子依赖性途径不太重要，并且存在显著的热稳定和热不稳定的非纤溶酶纤溶活性。这些可能包括参与补体激活以及经典和替代补体途径共同控制的蛋白酶，以及其他非纤溶酶蛋白酶。
