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Enhanced fibrinolytic activity during cardiopulmonary bypass in open‐heart surgery in man is caused by extrinsic (tissue‐type) plasminogen activator
Author(s) -
STIBBE JEANNE,
KLUFT CORNELIUS,
BROMMER EMILE J. P.,
GOMES MARIA,
JONG DICK S. DE,
NAUTA JAN
Publication year - 1984
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1984.tb01198.x
Subject(s) - plasminogen activator , cardiopulmonary bypass , fibrin , tissue plasminogen activator , fibrinogen , fibrinolysis , activator (genetics) , chemistry , medicine , t plasminogen activator , endocrinology , immunology , receptor
Abstract. The nature of the enhanced blood fibrinolytic activity which is known to occur during cardiopulmonary bypass is not understood. We show here that the cause is an increase in extrinsic (tissue‐type) plasminogen activator. In six patients, the nature of the enhanced blood fibrinolytic activity that evolved during cardiopulmonary bypass was characterized by differential inhibition using the fibrin plate method and was shown to be C1‐inactivator‐resistant (extrinsic‐activator activity). The C1‐inactivator‐resistant‐activator activity was completely quenched by an antibody against extrinsic (tissue‐type) plasminogen activator but not by antiurokinase, proving that the activity was due to the presence of extrinsic (tissue‐type) plasminogen activator. The concentration of extrinsic (tissue‐type) plasminogen activator increased during cardiopulmonary bypass and disappeared rapidly thereafter. Fibrinogen, plasminogen and α 2 ‐antiplasmin were not consumed during cardiopulmonary bypass, while no increase or occasionally a moderate one in fibrinogen degradation products occurred. This is in accord with the property of extrinsic (tissue‐type) plasminogen activator which activates plasminogen predominantly at sites where fibrin is present and not in the free circulation.