title: Prostacyclin deficiency and reduced fetoplacental blood flow in pregnancy-induced hypertension and preeclampsia.
abstract: BACKGROUND
  Low endothelial generation of prostacyclin (PGI(2)) is a typical feature of pregnancy-induced hypertensive disorders. The aim of the current study was to establish whether changes in PGI(2) are accompanied by alterations in fetoplacental blood flow and to test the hypothesis that PGI(2) deficiency contributes to reduced fetoplacental perfusion in pregnancy-induced hypertension (PIH) and preeclampsia.
  
  
  METHODS
  The study included 11 women with normal pregnancies, 12 with PIH/preeclampsia, and 7 with otherwise complicated pregnancies. Fetoplacental blood flow was assessed both by umbilical artery Doppler sonography measuring the resistance index (RI) and by means of neonatal birth weight. PGI(2) formation was measured in umbilical arteries prepared immediately after birth. PGI(2), RI and birth weight were correlated with and without correction for gestational age. Furthermore, data from patients with PIH/preeclampsia were compared with normal pregnancies as controls.
  
  
  RESULTS
  A significant inverse correlation was found between umbilical PGI(2) formation and umbilical RI and between birth weight and RI, whereas PGI(2) and birth weight were directly related. Patients with PIH/preeclampsia showed reduced PGI(2) formation, markedly increased gestational age-corrected RI and significantly reduced percentile birth weight.
  
  
  CONCLUSIONS
  These results provide evidence showing that PGI(2) is a relevant mediator of fetoplacental blood flow and suggest an important role of PGI(2) deficiency in PIH/preeclampsia.
authors.affiliation: Department of Obstetrics and Gynecology, Heinrich Heine University, Düsseldorf, Germany.
authors.forename: W
authors.initials: W
authors.lastname: Klockenbusch
authors.forename: T W
authors.initials: TW
authors.lastname: Goecke
authors.forename: J S
authors.initials: JS
authors.lastname: Krüssel
authors.forename: B A
authors.initials: BA
authors.lastname: Tutschek
authors.forename: G
authors.initials: G
authors.lastname: Crombach
authors.forename: K
authors.initials: K
authors.lastname: Schrör
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D001724:Birth Weight; D011464:Epoprostenol / Q000172:deficiency*; D005260:Female; D005333:Fetus / Q000098:blood supply*; D005865:Gestational Age; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D010920:Placenta / Q000098:blood supply*; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000503:physiopathology*; D014463:Ultrasonography; D014469:Umbilical Arteries / Q000000981:diagnostic imaging / Q000378:metabolism; D014655:Vascular Resistance
chemical_list: D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol