Acute endothelial tissue plasminogen activator release in pregnancy

• Published in: Journal of thrombosis and haemostasis 2009-01, Vol.7 (1), p.138-142
• Main Authors: ROBB, A. O., MILLS, N. L., DIN, J. N., CAMERON, S., LUDLAM, C. A., NEWBY, D. E., DENISON, F. C.
• Format: Article
• Language: English
• Subjects: Bradykinin - pharmacology; Case-Control Studies; Endothelium; Female; Fibrinolysis; Gravidity; Humans; Plasminogen Activator Inhibitor 1 - blood; Pregnancy; Pregnancy Trimester, Third; Regional Blood Flow; Thrombosis - etiology; Tissue Plasminogen Activator - metabolism; vascular biology
• ISSN: 1538-7933; 1538-7836; 1538-7836
• DOI: 10.1111/j.1538-7836.2008.03207.x

Objective: Pregnancy is associated with marked changes in vascular physiology and an increased risk of thrombosis. The aim of the study was to assess the effect of pregnancy on the acute release of tissue plasminogen activator (t‐PA) from the endothelium. Methods and results: Ten primigravida pregnant women were recruited in the third trimester of pregnancy (week 36 ± 1) and compared with 20 age‐matched non‐pregnant women (day 9.8 ± 0.3 of menstrual cycle). Blood flow and plasma fibrinolytic factors were measured in both forearms by venous occlusion plethysmography and blood sampling, respectively, during unilateral brachial artery infusions of bradykinin (100–1000 pmol min−1). Pregnant women had higher plasma plasminogen activator inhibitor type 1 (PAI‐1) antigen concentrations (77.1 ± 12.4 vs. 21.5 ± 9.8 ng mL−1; P = 0.004) that resulted in lower basal t‐PA/PAI‐1 ratios (0.2 ± 0.1 vs. 0.6 ± 0.1; P = 0.02) and plasma t‐PA activity concentrations (0.17 ± 0.02 vs. 0.58 ± 0.06 IU mL−1; P