Abstract
Marked changes in the hemostasis system, especially increases in PAI-2, are observed during pregnancy and at delivery. This inhibitor is produced by placental trophoblasts and by macrophages. PAI-2 occurs in two forms, a LMW and a HMW form. LMW PAI-2 is intracellular, HMW PAI-2 is secreted. PAI-2 inhibits both u-PA and two-chain t-PA. PAI-2 seems to be involved in the processes of invasion and remodeling of fetal and uterine tissues. It may protect against premature placental separation and secure hemostasis at parturition. Excess levels of PAI-2 in amniotic fluid may protect membranes from premature rupture. An imbalance between fibrinolytic activators and inhibitors may also be related to intracranial hemorrhage in premature infants. During preeclampsia t-PA and PAI-1 levels are markedly increased in plasma, and in cases of intrauterine growth retardation, u-PA and PAI-2 levels are decreased. While elevated PAI-1 concentrations might be helpful markers of severity of preeclampsia, decreased PAI-2 levels seem to indicate decreased placental function and intrauterine growth retardation.
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