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Abnormal fibrinolysis in healthy male cigarette smokers: Role of plasminogen activator inhibitors
Author(s) -
Haire William D.,
Goldsmith Jonathan C.,
Rasmussen Julie
Publication year - 1989
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830310107
Subject(s) - fibrinolysis , plasminogen activator , medicine , endocrinology , plasminogen activator inhibitor 1 , tissue plasminogen activator , immunology
Abstract The extrinsic fibrinolytic system and its response to cigarette smoking was studied in five healthy male smokers 35–45 years old. Tissue plasminogen activator (t‐PA) release in response to venous occlusion was intact both at 8:00 A.M. and 3:00 P.M. Acutely smoking two cigarettes neither stimulated fibrinolysis nor changed levels of t‐PA or plasminogen activator inhibitors. Functional plasminogen activator inhibitor (PA‐I) levels and euglobulin lysis times were higher in the smoking group than in a control group matched for age, sex, and body mass. Antigenic levels of PA‐I 1, the PA‐I derived from vascular endothelial cells and platelets, were similar in both groups. While smoking did not acutely alter fibrinolysis in chronic smokers, these individuals had a high frequency of abnormal fibrinolysis characterized by high levels of PA‐I activity. This abnormality is due to either high specific activity of PA‐I 1 or to the presence of other antigenically distinct plasminogen activator inhibitors. Abnormal firbinolysis may be one mechanism contributing to the thrombotic diathesis of cigarette smokers.