Author/Editor		Šabovič, M
Title		Mehanizem fiziološkega in farmakološkega raztapljanja krvnih strdkov
Type		monografija
Place		Ljubljana
Publisher		Medicinska fakulteta
Publication year		1992
Volume		str. 96
Language		slo
Abstract		Thrombolytic agents produce clot lysis by conversion of a proenzyme plasminogen (pIg) irtto an active enzyme plasmin, which degrades fibrin network of thrombi. Because a mechanism of lysis is very difficult to study in vivo, it has been studied in vitro by using nonretracted clots. In our previous study we observed that retracted clots lysed in a different way than nonretracted clots. Because of that, we decided to study the mechanism of lysis by using retracted clots, which has not been done yet. The retracted and nonretracated plasma and whole blood clots and also the ex-vivo thrombi were Iysed in both a plasma and buffer millieu. The lysis without (physiologic lysis) and with activator (pharmacologic lysis) were studied. The lysis of laboratory clots was followed.by measurements of 125-I fibrin degradation products, whereas the lysis of ex-vivo thrombi was followed by measurements of thrombi weight. The following activators were used: tissue-type plasminogen activator (t-PA), prourokinase (scu-PA), urokinase (UK) and streptokinase (SK). In order to find out the exact mechanism of lysis we measured the amount of plg in the clots and in plasma before lysis and during it. By using 125-I fibrin,131-I p1g and 131-J t-PA the parallel measurements of lysis and binding of plg and t-PA to clots was allowed. In the first study the mechanism of physiologic (spontaneous) Iysis was studied. It is well known that clots spontaneously lyse in plasma without activator. We found that lysis depends on the binding of plg and t-PA from surrounding plasma on clots; the binding of plg increased the dysability of clots, whereas the binding of t-PA increased the rate of lysis. Plg and t-PA bound on new binding sites exposed on partially degradated fibrin. We also measured that extrinsic t-PA (t-PA unbound in plasma) and not intrinsic t-PA (t-PA bound in clot) was responsible for the spontaneous lysis.(trunc.)
Descriptors		FIBRINOLYSIS THROMBOLYTIC THERAPY THROMBOSIS FIBRINOLYTIC AGENTS PLASMINOGEN ACTIVATORS PLASMINOGEN RADIOLIGAND ASSAY ALTEPLASE UROKINASE STREPTOKINASE