The postoperative fibrinolytic shutdown: a rapidly reverting acute phase pattern for the fast-acting inhibitor of tissue-type plasminogen activator after trauma

SummaryWe determined during the acute stage of myocardial infarction selected fibrinolysis variables (tissue-type plasminogen activator, intrinsic plasminogen activators, tissue-type plasminogen activator inhibition, C1-inactivator) and relatedthe observed changes to changes in two acute phase reactants (C-reactive protein, fibrinogen). Acute myocardial injury induce significant increases in blood of tissue-type plasminogen activator inhibition (day one, p <0.05), C-reactive protein (day three, p <0.01), fibrinogen (day six, p <0.01), and C1-inactivator (day eight, p <0.01). Tissue-type plasminogen activator activity measured as C1-inactivator resistant fibrinolytic activity showed a minimum day two after the acute attack (p <0.01), whereas plasminogen activator activities arising from the intrinsic system of fibrinolysis remained constant. The observed changes did not parallel the occurrence of deep vein thrombosis indicated by a positive Tc-plasmin test (41% of the patients).

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Modulation of Rapid Plasminogen Activator Inhibitor in Plasma by Stanozolol

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661110 ◽

1984 ◽

Vol 51 (03) ◽

pp. 396-397 ◽

Cited By ~ 40

Author(s):

J H Verheijen ◽

D C Rijken ◽

G T G Chang ◽

F E Preston ◽

C Kluft

Keyword(s):

Oral Administration ◽

Plasminogen Activator ◽

Fibrinolytic Activity ◽

Plasminogen Activator Inhibitor ◽

Tissue Type ◽

Tissue Type Plasminogen Activator ◽

Type Plasminogen Activator ◽

Fast Acting ◽

Activator Inhibitor

SummaryFibrinolytic activity in plasma euglobulin fractions can be increased by oral administration of stanozolol. This increase is not caused by increased synthesis or release of tissue-type plasminogen activator. A decreased level of fast acting t-PA inhibition is very probably the cause of the higher activity. These results suggest that this inhibition has a regulatory role on fibrinolysis in vivo.

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Daytime Fluctuations in Blood of Tissue-Type Plasminogen Activator (t-PA) and Its Fast-Acting Inhibitor (PAI-1)

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642781 ◽

1988 ◽

Vol 59 (02) ◽

pp. 329-332 ◽

Cited By ~ 125

Author(s):

C Kluft ◽

A F H Jie ◽

D C Rijken ◽

J H Verheijen

Keyword(s):

Plasminogen Activator ◽

Fibrinolytic Activity ◽

Tissue Type ◽

Tissue Type Plasminogen Activator ◽

Time Period ◽

Type Plasminogen Activator ◽

Circadian Fluctuation ◽

Fast Acting ◽

Pai 1

SummaryCircadian fluctuation in blood fibrinolytic activity was studiedin 10 volunteers in the day-time period at 09.00, 12.00 and15.0 h. Activity of tissue-type plasminogen activator (t-PA) wasfound to increase from 09.00 to 15.00 h in accordance with knownresults with global assays of blood activity.

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Hepatic Clearance of Tissue-Type Plasminogen Activator in Rats

Thrombosis and Haemostasis ◽

10.1055/s-0038-1660092 ◽

1985 ◽

Vol 54 (03) ◽

pp. 661-664 ◽

Cited By ~ 56

Author(s):

J J Emeis ◽

C M van den Hoogen ◽

D Jense

Keyword(s):

Plasminogen Activator ◽

Liver Perfusion ◽

Liver Blood Flow ◽

Hepatic Clearance ◽

Tissue Type ◽

Functional Assay ◽

Tissue Type Plasminogen Activator ◽

Type Plasminogen Activator ◽

Fast Acting ◽

Isolated Liver

SummaryThe clearance of tissue-type plasminogen activator (t-PA) was studied, in rats, by use of a functional assay for t-PA. Half-lives in the circulation were about one minute both for human (melanoma cell-derived) t-PA and for the rat’s own t-PA. The clearance of t-PA required an intact liver blood flow. In isolated liver perfusion experiments the hepatic extraction of t-PA did not require any plasma proteins, including fast-acting t-PA inhibitor. Competition experiments, using monosaccharides, suggested that known hepatic glycoprotein receptors were not involved in hepatic t-PA extraction.

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The Fast-Acting Inhibitor of Tissue-Type Plasminogen Activator in Plasma Is also the Primary Plasma Inhibitor of Urokinase

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661449 ◽

1986 ◽

Vol 55 (01) ◽

pp. 065-069 ◽

Cited By ~ 53

Author(s):

Egbert K.O Kruithof ◽

Chiên Tran-Thang ◽

Fedor Bachmann

Keyword(s):

Plasminogen Activator ◽

Plasminogen Activator Inhibitor ◽

Order Rate Constant ◽

Tissue Type ◽

Subsequent Formation ◽

Prolonged Incubation ◽

Tissue Type Plasminogen Activator ◽

Type Plasminogen Activator ◽

Fast Acting ◽

Activator Inhibitor

SummaryWe have compared the ability of a plasminogen activator inhibitor (PA-inhibitor) in human plasma, to form complexes with radioiodinated tissue-type plasminogen activator (t-PA) and high molecular weight urokinase (HMr-UK). Addition of 125I-t-PA (final concentration 10 IU/ml) or of 125I-HMr-UK (2 IU/ml) to a plasma containing 33 U/ml of PA-inhibitor resulted in the rapid formation of a 110,000 Mr complex of 125I-t-PA or a 95,000 Mr complex of 125I-HMr-UK with PA-inhibitor. Upon prolonged incubation of the plasma with 125I-HMr-UK a secondary complex of a Mr of 88,000 was observed, which probably derives from limited degradation of the 95,000 complex. Preincubation of the plasma with unlabelled t-PA, HMr-UK or LMr-UK at higher concentrations prevented the subsequent formation of complexes between radiolabelled PAs and the PA-inhibitor. These results thus demonstrate that t-PA and UK form complexes with the same PA-inhibitor. The rate of complex formation of 125I-t-PA or of 125I-HMr-UK with the plasma PA-inhibitor was similar (second order rate constant of association with PA-inhibitor in the order of 107 M−1s−1).

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