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Activation of coagulation and fibrinolytic systems following stroke
Author(s) -
Lane D. A.,
Wolff S.,
Ireland H.,
Gawel M.,
Foadi M.
Publication year - 1983
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1983.tb07316.x
Subject(s) - plasmin , fibrin , thrombin , medicine , coagulation , platelet , stroke (engine) , fibrinolysis , platelet activation , protease , endocrinology , immunology , chemistry , biochemistry , enzyme , mechanical engineering , engineering
S ummary . When the human blood coagulation and fibrinolytic systems are activated thrombin cleaves fibrinopeptide A (FPA) and plasmin cleaves Bβ1‐42 from fibrin(ogen). Elevated plasma concentrations of FPA and Bβ1‐42 are evidence for enhanced thrombin and plasmin activities in plasma. We have determined the plasma concentrations of FPA and Bβ1‐42 in patients who have had thrombotic stroke. Patients who were studied immediately following stroke were found to have greatly elevated plasma FPA and Bβ1‐42 levels, but these decreased to the concentrations found in an apparently healthy age‐matched control group 1 month after the infarct. In contrast, the plasma concentrations of the platelet release product β‐thromboglobulin (βTG) were slightly, but significantly, elevated immediately following the stroke and these did not alter with time after the infarct. It is concluded that following thrombotic stroke increased thrombin and plasmin activities are to be found in plasma. These increased protease activities are probably not directly associated with an increased in vivo platelet release reaction and may be useful in deciding which patients are at risk of reinfarction or stroke progression.