OBJECTIVE: The purpose of this study was to evaluate the plasminogen activator system in maternal and umbilical cord plasma in patients with severe preeclampsia compared with control subjects with normotensive pregnancies. STUDY DESIGN: Maternal blood was sampled from 42 patients at a median gestational age of 32 weeks; after delivery, arterial and venous umbilical cord blood was sampled from 37 and 36 of these patients, respectively. Maternal blood from women with uncomplicated pregnancies was sampled at the gestational age of 32 weeks (n = 18, group I), and umbilical cord blood was sampled after premature deliveries of normotensive pregnancies (n = 5, group II). Data were analyzed with the use of Mann-Whitney U tests. RESULTS: Patients had significantly higher tissue plasminogen activator (P <.01) and unchanged urokinase plasminogen activator plasma levels compared with control subjects at 32 weeks of gestation; lower plasminogen activator inhibitor type 2 (P < 0.01) and no different plasminogen activator inhibitor type 1 concentrations were observed compared to control subjects at 32 weeks of gestation. In the arterial and venous umbilical cord plasma of patients, plasminogen activator inhibitor type 1 levels were significantly higher(P <.01) compared with control subjects at 32 weeks of gestation, although urokinase plasminogen activator levels in arterial and venous umbilical cord plasma (P < 0.01) were significantly lower. CONCLUSION: Lower plasminogen activator inhibitor type 2 levels are associated with placental insufficiency, and higher tissue plasminogen activator levels are associated with endothelial dysfunction in patients with severe preeclampsia. The higher plasminogen activator inhibitor type 1 levels and lower urokinase plasminogen activator levels in umbilical cord of these patients are suggestive of decreased fibrinolysis in the fetal circulation.
OBJECTIVE: The purpose of this study was to evaluate the plasminogen activator system in maternal and umbilical cord plasma in patients with severe preeclampsia compared with control subjects with normotensive pregnancies. STUDY DESIGN: Maternal blood was sampled from 42 patients at a median gestational age of 32 weeks; after delivery, arterial and venous umbilical cord blood was sampled from 37 and 36 of these patients, respectively. Maternal blood from women with uncomplicated pregnancies was sampled at the gestational age of 32 weeks (n = 18, group I), and umbilical cord blood was sampled after premature deliveries of normotensive pregnancies (n = 5, group II). Data were analyzed with the use of Mann-Whitney U tests. RESULTS:Patients had significantly higher tissue plasminogen activator (P <.01) and unchanged urokinase plasminogen activator plasma levels compared with control subjects at 32 weeks of gestation; lower plasminogen activator inhibitor type 2 (P < 0.01) and no different plasminogen activator inhibitor type 1 concentrations were observed compared to control subjects at 32 weeks of gestation. In the arterial and venous umbilical cord plasma of patients, plasminogen activator inhibitor type 1 levels were significantly higher(P <.01) compared with control subjects at 32 weeks of gestation, although urokinase plasminogen activator levels in arterial and venous umbilical cord plasma (P < 0.01) were significantly lower. CONCLUSION: Lower plasminogen activator inhibitor type 2 levels are associated with placental insufficiency, and higher tissue plasminogen activator levels are associated with endothelial dysfunction in patients with severe preeclampsia. The higher plasminogen activator inhibitor type 1 levels and lower urokinase plasminogen activator levels in umbilical cord of these patients are suggestive of decreased fibrinolysis in the fetal circulation.