Die Bedeutung des Proaktivators im fibrinolytischen Fermentsystem

Spöttl, F; Constantini, R.

doi:10.1055/s-0038-1655050

Cited by 3 publications

(2 citation statements)

References 10 publications

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“…-releases 7.5 µg tyrosine/min. The method is fully described elsewhere (39,40). The difference between the plasminogen level before and the mean of the 45 and 60 min sample after SK.…”

mentioning

confidence: 99%

The Influence of Inhibitors of Plasmin and Plasminogen Activation on the Streptokinase-Induced Fibrinolytic State

Spöttl¹,

Holzknecht²

1970

Thromb Haemost

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SummaryThe influence of the inhibitors of plasminogen activation by streptokinase, urokinase and tissue activator and of the two antiplasmins i.e. α1 antitrypsin and α2-macroglobulin, upon the formation and clearance of streptokinase-activator in vivo was investigated in 22 subjects. No influence of the above mentioned inhibitors on the formation of the streptokinase-activator could be found, whereas the clearance of the activator seems to be a function of the α2-macroglobulin level before streptokinase administration. The clearance rate of the streptokinase-activator differed significantly from the clearance rate of 131I labelled streptokinase caused by antigen-antibody complex formation [Fletcher et al. (10)], and was similar to the clearance rate of the histamine or nicotinic acid induced plasminogen activator. The possibility of a common clearing mechanism of fibrinolytic activators is discussed.The existence of 3 different inhibitors activities on plasminogen activation as tested in vitro i. e. inhibitor of streptokinase, urokinase and tissue activator, was demonstrated. These inhibitory activities are probably not the properties of 3 different serum proteins but rather the result of the action of α1antitrypsin and α2-macroglobulin. The degree of inhibition, however, of each of the 2 proteins on each of the 3 plasminogen activators (streptokinase, urokinase and tissue activator) seems to be different. This difference may be caused by a different inhibitory effect of α1 antitrypsin or α2-macroglobulin on each of the plasminogen activators.The plasmin formed after the streptokinase infusion is rapidly bound by the α2macroglobulin and this plasmin-antiplasmin complex is immediately removed from the blood, causing a decrease of the α2-macroglobulin level. This decrease of α2-macroglobulin is correlated with the initial level of α2-macroglobulin. This finding demonstrates the concentration depending formation of the plasmin-antiplasmin complex also in vivo.

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“…-releases 7.5 µg tyrosine/min. The method is fully described elsewhere (39,40). The difference between the plasminogen level before and the mean of the 45 and 60 min sample after SK.…”

mentioning

confidence: 99%

The Influence of Inhibitors of Plasmin and Plasminogen Activation on the Streptokinase-Induced Fibrinolytic State

Spöttl¹,

Holzknecht²

1970

Thromb Haemost

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“…Plasminogen was determined using a caseinolytic method (24) but euglobulins were used instead of plasma. T his modification was done in order to discard t h e retained metabolites t hat might have interfered with the estimation of acid soluble tyrosine produced by proteolysis in vitro.…”

Section: Methodsmentioning

confidence: 99%

Disseminated Intravascular Coagulation and Acute Renal Failure

Crîsnic¹,

Cucuianu²,

Manasia³

et al. 1971

Thromb Haemost

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SummaryStarting from a hypothesis according to which disseminated intravascular coagulation might be an intermediary mechanism in the production of acute renal failure, investigations were made in 94 cases of anuria of different etiology, in order to detect signs of a consumption coagulopathy. After an average lapse of time of 48 h since the onset of anuria, the most frequently encountered hemostatic defect was a decreased platelet adhesiveness. In vitro experiments and clinical observations suggest that in the early stage of acute renal failure caused by a septic abortion, deficient platelet adhesiveness is due, mainly to platelet damage caused by intravascular coagulation or by bacterial toxins and not by the retention of metabolites. Euglobulin lysis time was prolonged, but a significant decrease of the plasminogen level indicates that an activation of fibrinolysis might have occured in the evolution of the process.

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