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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1992-7-28
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pubmed:abstractText |
Thrombolytic therapy frequently induces a "lytic state" associated with a decrease in plasma plasminogen concentration that could limit therapeutic efficacy. We therefore investigated the influence of soluble plasminogen concentration on in vitro lysis of retracted whole-blood clots in plasma from normal subjects and from patients undergoing thrombolytic therapy. With recombinant tissue plasminogen activator (1000 ng/ml) or two-chain urokinase plasminogen activator (250 U/ml), minimal clot lysis occurred in normal plasma depleted of plasminogen by lysine Sepharose chromatography. Clot lysis induced by two-chain urokinase plasminogen activator increased progressively in normal plasma at initial plasminogen concentrations between 0.06 to 6 U/ml, whereas maximum lysis with recombinant tissue plasminogen activator occurred between 0.5 U/ml and 1 U/ml and was less at lower and higher concentrations of plasminogen. Incubation of whole-blood clots in normal plasma with recombinant tissue plasminogen activator resulted in little change in plasminogen concentration during 6 hours, with a constant rate of clot lysis. Incubation with two-chain urokinase plasminogen activator, however, caused a rapid decrease in plasminogen concentration and a corresponding decrease in lysis rate; lysis rate was restored after repletion with purified plasminogen. The effect of in vivo activator-induced plasminogen depletion on in vitro clot lysis rates was tested with plasma obtained from patients 90 to 120 minutes after they had received 30 mg of acylated plasminogen-streptokinase activator complex that showed depletion of plasminogen to 14% +/- 2%. These plasma samples produced only 4% +/- 1% in vitro clot lysis during 4 hours but lysis increased progressively after repletion with 1, 2, and 4 U/ml plasminogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Plasminogen,
http://linkedlifedata.com/resource/pubmed/chemical/Plasminogen Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tissue Plasminogen Activator,
http://linkedlifedata.com/resource/pubmed/chemical/Urokinase-Type Plasminogen Activator
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-2143
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
120
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
120-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:1613318-Blood Coagulation,
pubmed-meshheading:1613318-Fibrinolysis,
pubmed-meshheading:1613318-Humans,
pubmed-meshheading:1613318-Plasminogen,
pubmed-meshheading:1613318-Plasminogen Activators,
pubmed-meshheading:1613318-Recombinant Proteins,
pubmed-meshheading:1613318-Thrombolytic Therapy,
pubmed-meshheading:1613318-Tissue Plasminogen Activator,
pubmed-meshheading:1613318-Urokinase-Type Plasminogen Activator
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pubmed:year |
1992
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pubmed:articleTitle |
Depletion of plasminogen in vitro or during thrombolytic therapy limits fibrinolytic potential.
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pubmed:affiliation |
Department of Medicine, University of Rochester School of Medicine and Dentistry, New York.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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