Abstract
<h2>Abstract</h2> The mechanism underlying the effect of dextran on the lysis of plasma clots was studied. With the aid of <sup>125</sup>I-plasminogen, the formation of radiolabelled derivatives of urokinase-induced plasminogen activation was followed in clotted plasma. The activation was enhanced by the presence of dextran, but the rate of formation of the complex between plasmin and α<sub>2</sub>-antiplasmin was not. By measuring the amount of plasmin activity remaining after addition of plasmin and α<sub>2</sub>-antiplasmin to clots or fibrinogen solutions, it was found that in purified fibrin clots the α<sub>2</sub>-antiplasmin activity was impaired in the presence of dextran. In fibrinogen solutions dextran appeared to have no effect on the α<sub>2</sub>-antiplasmin activity. It is concluded that two different mechanisms are involved in the dextran-induced improvement of plasma clot lysis - an increased plasminogen activation rate and decreased α<sub>2</sub>-antiplasmin activity. The latter effect is apparently dependent on the morphologically different type of fibrin formed in the presence of dextran.
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