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Heparin inhibits spontaneous thrombolysis and the thrombolytic effect of both streptokinase and tissue‐type plasminogen activator. An in vitro study of the dislodgement of platelet‐rich thrombi formed from native blood
Author(s) -
GÖRÖG P.,
RIDLER C. D.,
KOVACS I. B.
Publication year - 1990
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.1990.tb00130.x
Subject(s) - heparin , medicine , streptokinase , thrombolysis , thrombus , platelet , plasminogen activator , tissue plasminogen activator , t plasminogen activator , myocardial infarction , pharmacology , plasmin , cardiology , chemistry , biochemistry , enzyme
. Two in vitro models of coronary thrombolysis in man, i.e. dislodgement of thrombi formed from non‐anticoagulated human blood, either by (i) shear‐stress or (ii) interaction of platelets with type I collagen fibre, were studied. Heparinization (1 U/ml) of blood prior to thrombus formation by (i) strongly inhibited spontaneous dislodgement ( P < 0.0001). Heparin (1 U/ml), when added with streptokinase (SK) or tissue‐type plasminogen activator (rt‐PA) prior to thrombus formation, considerably delayed thrombolysis. Furthermore, thrombolysis occurred much earlier when thrombi were perfused with SK or rt‐PA in native than in heparinized blood. Heparin inhibited binding of 125 I‐rt‐PA (17%, P < 0.02) and plasminogen (88%, P < 0.0005) to platelets activated by ADP in citrated platelet‐rich plasma. We conclude that heparin interferes with the fibrinolytic system at the surface of activated platelets. Our findings suggest that heparin administration prior to thrombolytic therapy for acute myocardial infarction should be questioned.