Abnormal fibrinolysis in healthy male cigarette smokers: Role of plasminogen activator inhibitors

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 fibrinolysis may be one mechanism contributing to the thrombotic diathesis of cigarette smokers.