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dc.contributor.authorOnundarson, P T
dc.contributor.authorHaraldsson, H M
dc.contributor.authorBergmann, L
dc.contributor.authorFrancis, C W
dc.contributor.authorMarder, V J
dc.date.accessioned2011-02-16T11:45:46Z
dc.date.available2011-02-16T11:45:46Z
dc.date.issued1993-12-20
dc.date.submitted2011-02-16
dc.identifier.citationThromb. Haemost. 1993, 70(6):998-1004en
dc.identifier.issn0340-6245
dc.identifier.pmid8165625
dc.identifier.urihttp://hdl.handle.net/2336/122057
dc.description.abstractThe relationship between lytic state variables and ex vivo clot lysability was investigated in blood drawn from patients during streptokinase administration for acute myocardial infarction. A lytic state was already evident after 5 min of treatment and after 20 min the plasminogen concentration had decreased to 24%, antiplasmin to 7% and fibrinogen 0.2 g/l. Lysis of radiolabeled retracted clots in the patient plasmas decreased from 37 +/- 8% after 5 min to 21 +/- 8% at 10 min and was significantly lower (8 +/- 9%, p < 0.005) in samples drawn at 20, 40 and 80 min. Clot lysability correlated positively with the plasminogen concentration (r = 0.78, p = 0.003), but not with plasmin activity. Suspension of radiolabeled clots in normal plasma pre-exposed to 250 U/ml two-chain urokinase for varying time to induce an in vitro lytic state was also associated with decreasing clot lysability in direct proportion with the duration of prior plasma exposure to urokinase. The decreased lysability correlated with the time-dependent reduction in plasminogen concentration (r = 0.88, p < 0.0005). Thus, clot lysability decreases in conjunction with the development of the lytic state and the associated plasminogen depletion. The lytic state may therefore limit reperfusion during thrombolytic treatment.
dc.language.isoenen
dc.subject.meshAmino Acid Sequenceen
dc.subject.meshHumansen
dc.subject.meshInfusions, Intravenousen
dc.subject.meshIodine Radioisotopesen
dc.subject.meshMolecular Sequence Dataen
dc.subject.meshMyocardial Infarctionen
dc.subject.meshPlasminogenen
dc.subject.meshStreptokinaseen
dc.subject.meshThrombolytic Therapyen
dc.subject.meshThrombophlebitisen
dc.subject.meshUrokinase-Type Plasminogen Activatoren
dc.titlePlasminogen depletion during streptokinase treatment or two-chain urokinase incubation correlates with decreased clot lysability ex vivo and in vitroen
dc.typeArticleen
dc.contributor.departmentDepartment of Hematology, Landspítalinn University Hospital, Reykjavík, Iceland.en
dc.identifier.journalThrombosis and haemostasisen
html.description.abstractThe relationship between lytic state variables and ex vivo clot lysability was investigated in blood drawn from patients during streptokinase administration for acute myocardial infarction. A lytic state was already evident after 5 min of treatment and after 20 min the plasminogen concentration had decreased to 24%, antiplasmin to 7% and fibrinogen 0.2 g/l. Lysis of radiolabeled retracted clots in the patient plasmas decreased from 37 +/- 8% after 5 min to 21 +/- 8% at 10 min and was significantly lower (8 +/- 9%, p < 0.005) in samples drawn at 20, 40 and 80 min. Clot lysability correlated positively with the plasminogen concentration (r = 0.78, p = 0.003), but not with plasmin activity. Suspension of radiolabeled clots in normal plasma pre-exposed to 250 U/ml two-chain urokinase for varying time to induce an in vitro lytic state was also associated with decreasing clot lysability in direct proportion with the duration of prior plasma exposure to urokinase. The decreased lysability correlated with the time-dependent reduction in plasminogen concentration (r = 0.88, p < 0.0005). Thus, clot lysability decreases in conjunction with the development of the lytic state and the associated plasminogen depletion. The lytic state may therefore limit reperfusion during thrombolytic treatment.


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