Maternal tissue blood flow and oxygen saturation in pre-eclampsia and intrauterine growth restriction.

OBJECTIVE: To investigate the hypothesis that impaired maternal tissue perfusion occurs in pre-eclampsia and intrauterine growth restriction (IUGR) and this correlates with maternal tissue oxygenation. STUDY DESIGN: Strain gauge plethysmography was used to compare maternal calf blood flow during the third trimester in 16 women with pre-eclampsia, 6 women with IUGR and 16 normal pregnant controls. A Mediaid iPOX pulse oximeter was used to measure maternal tissue oxygenation in the three groups and these were compared with tissue blood flow. RESULTS: Maternal tissue blood flow was significantly reduced in pre-eclampsia compared to the two other groups (p=0.003). Blood flow was significantly reduced in pre-eclampsia compared to IUGR (p=0.03). However there was no difference in blood flow between normal pregnancy and IUGR groups (p=0.76). No significant difference was noted in maternal tissue oxygenation between the normal pregnancy, pre-eclampsia and IUGR groups (mean±S.E.M. [97.13±0.4, 96.69±0.33, 97.83±0.47 respectively], p=0.26). No correlation was noted between blood flow and tissue oxygenation in the three groups of women. CONCLUSION: We have demonstrated that reduced maternal resting tissue blood flow present in women with pre-eclampsia is not seen in women with IUGR and the reduction in blood flow in pre-eclampsia is not associated with changes in maternal tissue oxygenation.

Placental angiogenin inhibitor (ribonuclease inhibitor), a novel gene in pre-eclampsia.

There is convincing evidence that imbalance between angiogenic and anti-angiogenic factors play an important role in the pathophysiology of pre-eclampsia. Angiogenin, a member of the RNase A super family, is a potent inducer of angiogenesis and serum levels are shown to be elevated in pre-eclampsia. We hypothesize that placental expression of angiogenin inhibitor which binds and blocks the activity of angiogenin is altered in pre-eclampsia and may play a role in its pathophysiology. Placental expression of angiogenin inhibitor was measured in term placentae of 15 women with preeclampsia and 16 normal pregnant controls. The women were matched for age, parity and gestational age. Placental tissue was collected immediately after delivery and stored at -80°C until studied. Angiogenin inhibitor gene expression was measured using real-time quantitative polymerase chain reaction (rt-QPCR). The results were standardized using the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as reference gene. The mRNA expression of angiogenin inhibitor gene was significantly increased in preeclamptic placentae compared to normal pregnant controls [0.44 (0.174-1.048) versus 0.091 (0.029-0.301), median and interquatile range, p=0.027 for pre-eclampsia and normal controls respectively]. There was no correlation between angiogenin inhibitor gene expression and maternal age, blood pressure, platelet count, gestation age, birth weight of the baby in pre-eclampsia and normal pregnancy. This study showed that placental expression of the angiogenin inhibitor gene is significantly increased in pre-eclampsia and may play a role in its pathophysiology.

PP011. Increased placental expression of angiogenin inhibitor (Ribonuclease inhibitor), a novel gene in pre-eclampsia.

INTRODUCTION: There is convincing evidence that imbalance between angiogenic and anti-angiogenic factors play an important role in the pathophysiology of pre-eclampsia. Increased expression of soluble fms-like tyrosine kinase-1 (sFlt1), along with decreased placental growth factor (PlGF) and vascular endothelial growth factor (VEGF) appear to play a key role in the abnormal placentation and vascular dysfunction of pre-eclampsia. Angiogenin is a potent inducer of angiogenesis and serum levels are elevated in pre-eclampsia. Angiogenin Inhibitor (also called placental Ribonuclease inhibitor) is a potent antagonist of both angiogenic and ribonucloetic activities of angiogenin. We demonstrate that placental expression of angiogenin inhibitor is altered in pre-eclampsia and may play a role in its pathophysiology. OBJECTIVES: The aim of the study was to assess the expression of angiogenin inhibitor in healthy normotensive and pre-eclamptic placentas. METHODS: Placental expression of angiogenin inhibitor was measured in term placentae of 14 pre-eclamptic women and 16 normal pregnant controls. The women were matched for age, gestation and parity. Placental tissue was collected immediately after delivery and stored at -80°C. The angiogenin inhibitor gene expression was measured using real-time quantitative polymerase chain reaction (rt-QPCR). The results were standardized using the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reference gene. RESULTS: mRNA expression of angiogenin inhibitor gene was significantly increased in pre-eclamptic placentae (p=0.027) compared to normal pregnant controls; 0.44 (0.174-1.048) versus 0.091 (0.029-0.301), median and interquartile range, for pre-eclampsia and normal controls, respectively. CONCLUSION: Placenta expression of angiogenin inhibitor gene is significantly increased in pre-eclampsia and may play a role in its pathophysiology. This finding may directly correlate with the reported ability of angiogenin inhibitor to protect from oxidative stress by its reactivity as an oxygen species scavenger.