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dc.contributor.authorMagnús Haraldsson
dc.contributor.authorPáll Torfi Önundarson
dc.contributor.authorLena Bergmann
dc.date.accessioned2009-08-26T10:00:12Z
dc.date.available2009-08-26T10:00:12Z
dc.date.issued1993-10-01
dc.date.submitted2009-08-26
dc.identifier.citationLæknablaðið 1993, 79(8):297-304en
dc.identifier.issn0023-7213
dc.identifier.urihttp://hdl.handle.net/2336/78596
dc.descriptionNeðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/Openen
dc.description.abstractThrombolytic therapy is associated with the development of a lytic state manifested by depletion of fibrinogen, coagulation factors V and VIII, plasminogen and antiplasmin to a varying degree. The severity of the lytic state is dependent on the type and dose of plasminogen activator applied and is frequently considered desirable 303 during treatment as a measurable indicator of effective in vivo fibrinolysis and an important hypocoagulable condition preventing reocclusion after thrombolytic therapy. However, in vitro data indicate that more clot can be lysed using rt-PA which causes less lytic state than urokinase (tcu-PA, UK) which induces a more pronounced lytic state and that this may possibly be explained in part by depletion of circulating (rather than clot-bound) plasminogen. Based on this hypothesis we have investigated the speed and intensity of lytic state formation in 6 patients treated with 1.500.000 units of streptokinase over one hour for acute myocardial infarction by drawing blood at consecutive early timepoints during infusion. Already after 10 minutes of infusion the plasminogen concentration had decreased to 47±6% of initial, 24±4% after 20 minutes and <15% after 40 and 80 minutes. Antiplasmin was 53±11% after 5 minutes, 19±5% after 10 minutes and about 5% at 20 minutes and therafter. Fibrinogen degradation was also rapid: 72±8% of initial at 10 minutes, 19±9% at 20 minutes and 6±1% after 40 and 80 minutes. A curvilinear relationship was found between the concentration changes of fibrinogen and plasminogen during therapy (R2=.94) making it possible to predict plasminogen concentration based on fibrinogen levels. It is concluded that near maximum lytic state developes within 10-20 minutes of streptokinase infusion for myocardial infarction. Although further study is needed it can be hypothesized based on these results and others' in vitro data that the rapid development of an intense lytic state may limit therapeutic success.
dc.description.abstractVeruleg eyðing margra plasmaprótína er komin fram einni og hálfri klukkustund eftir gjöf segaleysandi lyfja. Mæling leysiástands er oft talin vísbending þess að nægileg raeðferð hafi verið gefin til upplausnar blóðsega. Lyf, sem valda litlu leysiástandi (til dæmis rt-PA), eru þó að minnsta kosti jafnvirk þeim, sem valda miklu leysiástandi í klínískum rannsóknum (SK, APSAC, UK). Glasarannsóknir benda til sterkra tengsla á milli ensímatískrar storkuleysingar og styrks plasminogens í plasma. Markvissar mælingar á hversu hratt leysiástand myndast hafa hins vegar ekki verið gerðar á mönnum, með það fyrir augum að meta hvort segaleysing fari minnkandi með vaxandi leysiástandi og minnkandi þéttni plasminogens. Blóð var dregið úr sex sjúklingum sem fengu streptókínasa, (SK) 1.500.000 I.U. á 60 mínútum, vegna gruns um bráða kransæðastíflu. Sýni voru dregin fyrir upphaf meðferðar og síðan með stuttu millibili eftir að hún hófst (5, 10, 20, 40 og 80 mínútum eftir upphaf meðferðar). Mælt var magn plasminogens, andplasmíns og fibrinogens í plasma. Plasminogen reyndist minnkað í 47 ±7% af upphaflegu eftir 10 mínútur og 24±4% 20 mínútum eftir upphaf gjafar. Eftir 40 og 80 mínútur var plasminogen 15±1% og 10±1% af upphaflegu. Andplasmín var 53±11% eftir fimm mínútur, 19±5% eftir 10 mínútur og nánast uppurið eftir 20 mínútur. Þéttni fibrinogens minnkaði einnig fljótt, en þó heldur hægar en þéttni plasminogens. Fibrinogen var 72±8% af upphaflegu eftir 10 mínútur, 19±9% eftir 20 mínútur og 6±1% eftir 40 og 80 mínútur. Sterk fylgni (boglinuferill, R2=,94) fannst milli styrks fibrinogens og plasminogens meðan á SK-meðferð stóð.
dc.language.isoisen
dc.publisherLæknafélag Íslands, Læknafélag Reykjavíkuren
dc.relation.urlhttp://www.laeknabladid.isen
dc.subject.meshThrombolytic Therapyen
dc.subject.meshFibrinolytic Agenten
dc.titleMyndunarhraði leysiástands við gjöf streptókínasais
dc.typeArticleen
dc.identifier.journalLæknablaðiðen
refterms.dateFOA2018-09-12T18:18:03Z
html.description.abstractThrombolytic therapy is associated with the development of a lytic state manifested by depletion of fibrinogen, coagulation factors V and VIII, plasminogen and antiplasmin to a varying degree. The severity of the lytic state is dependent on the type and dose of plasminogen activator applied and is frequently considered desirable 303 during treatment as a measurable indicator of effective in vivo fibrinolysis and an important hypocoagulable condition preventing reocclusion after thrombolytic therapy. However, in vitro data indicate that more clot can be lysed using rt-PA which causes less lytic state than urokinase (tcu-PA, UK) which induces a more pronounced lytic state and that this may possibly be explained in part by depletion of circulating (rather than clot-bound) plasminogen. Based on this hypothesis we have investigated the speed and intensity of lytic state formation in 6 patients treated with 1.500.000 units of streptokinase over one hour for acute myocardial infarction by drawing blood at consecutive early timepoints during infusion. Already after 10 minutes of infusion the plasminogen concentration had decreased to 47±6% of initial, 24±4% after 20 minutes and <15% after 40 and 80 minutes. Antiplasmin was 53±11% after 5 minutes, 19±5% after 10 minutes and about 5% at 20 minutes and therafter. Fibrinogen degradation was also rapid: 72±8% of initial at 10 minutes, 19±9% at 20 minutes and 6±1% after 40 and 80 minutes. A curvilinear relationship was found between the concentration changes of fibrinogen and plasminogen during therapy (R2=.94) making it possible to predict plasminogen concentration based on fibrinogen levels. It is concluded that near maximum lytic state developes within 10-20 minutes of streptokinase infusion for myocardial infarction. Although further study is needed it can be hypothesized based on these results and others' in vitro data that the rapid development of an intense lytic state may limit therapeutic success.
html.description.abstractVeruleg eyðing margra plasmaprótína er komin fram einni og hálfri klukkustund eftir gjöf segaleysandi lyfja. Mæling leysiástands er oft talin vísbending þess að nægileg raeðferð hafi verið gefin til upplausnar blóðsega. Lyf, sem valda litlu leysiástandi (til dæmis rt-PA), eru þó að minnsta kosti jafnvirk þeim, sem valda miklu leysiástandi í klínískum rannsóknum (SK, APSAC, UK). Glasarannsóknir benda til sterkra tengsla á milli ensímatískrar storkuleysingar og styrks plasminogens í plasma. Markvissar mælingar á hversu hratt leysiástand myndast hafa hins vegar ekki verið gerðar á mönnum, með það fyrir augum að meta hvort segaleysing fari minnkandi með vaxandi leysiástandi og minnkandi þéttni plasminogens. Blóð var dregið úr sex sjúklingum sem fengu streptókínasa, (SK) 1.500.000 I.U. á 60 mínútum, vegna gruns um bráða kransæðastíflu. Sýni voru dregin fyrir upphaf meðferðar og síðan með stuttu millibili eftir að hún hófst (5, 10, 20, 40 og 80 mínútum eftir upphaf meðferðar). Mælt var magn plasminogens, andplasmíns og fibrinogens í plasma. Plasminogen reyndist minnkað í 47 ±7% af upphaflegu eftir 10 mínútur og 24±4% 20 mínútum eftir upphaf gjafar. Eftir 40 og 80 mínútur var plasminogen 15±1% og 10±1% af upphaflegu. Andplasmín var 53±11% eftir fimm mínútur, 19±5% eftir 10 mínútur og nánast uppurið eftir 20 mínútur. Þéttni fibrinogens minnkaði einnig fljótt, en þó heldur hægar en þéttni plasminogens. Fibrinogen var 72±8% af upphaflegu eftir 10 mínútur, 19±9% eftir 20 mínútur og 6±1% eftir 40 og 80 mínútur. Sterk fylgni (boglinuferill, R2=,94) fannst milli styrks fibrinogens og plasminogens meðan á SK-meðferð stóð.


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