title: Role of placental growth hormone in the alteration of maternal arterial resistance in pregnancy.
abstract: OBJECTIVE
  To investigate the relation between arterial resistance and placental growth hormone (hGH-V) levels in the maternal circulation.
  
  
  METHODS
  Sixty-seven women with normal pregnancy, 13 with preeclampsia (PE) and 11 with intrauterine fetal growth restriction (IUGR) underwent Doppler sonography of the placental and nonplacental uterine and cubital artery and blood sampling. hGH-V was measured with a highly sensitive sandwich-type immunofluorometric assay and pituitary growth hormone (hGH-N) and insulinlike growth factor I (IGF-I) with a chemiluminescence assay. A p value of < 0.05 was considered significant.
  
  
  RESULTS
  During normal pregnancy the arterial pulsatility index (PI) decreased (p < 0.001), serum levels of hGH-V and IGF-I increased (p < 0.0001), and hGH-N decreased (p < 0.0001). Pathologic pregnancies (PE, IUGR) showed a significant higher PI in all arteries, but hGH-V and the IGF-I were decreased.
  
  
  CONCLUSIONS
  Our data demonstrate a strong correlation between decreasing uterine and peripheral arterial resistance and increasing hGH-V during normal pregnancies with impaired uterine blood flow there were lowered serum levels of hGH-V, hGH-N and IGF-I. Lower levels of hGH-V and hGH-N might contribute to impaired uteroplacental circulation.
authors.affiliation: Prenatal Medicine Unit, Department of Obstetrics and Gynecology, Ludwig-Maximilians University, Munich, Germany. barbara.schiessl@med.uni-muenchen.de
authors.forename: Barbara
authors.initials: B
authors.lastname: Schiessl
authors.forename: Christian J
authors.initials: CJ
authors.lastname: Strasburger
authors.forename: Martin
authors.initials: M
authors.lastname: Bidlingmaier
authors.forename: Martin
authors.initials: M
authors.lastname: Bidlingmeier
authors.forename: Bodo
authors.initials: B
authors.lastname: Gutt
authors.forename: Susan E
authors.initials: SE
authors.lastname: Kirk
authors.forename: Renate
authors.initials: R
authors.lastname: Oberhoffer
authors.forename: Klaus
authors.initials: K
authors.lastname: Friese
mesh_terms: D000328:Adult; D001158:Arteries; D016022:Case-Control Studies; D005260:Female; D005317:Fetal Growth Retardation / Q000097:blood* / Q000503:physiopathology; D013006:Growth Hormone / Q000097:blood / Q000502:physiology*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D010920:Placenta / Q000098:blood supply*; D021041:Placental Circulation; D010926:Placental Hormones / Q000502:physiology*; D011225:Pre-Eclampsia / Q000097:blood* / Q000503:physiopathology; D011247:Pregnancy / Q000097:blood*; D012039:Regional Blood Flow; D018617:Ultrasonography, Doppler, Pulsed / Q000379:methods; D014599:Uterus / Q000098:blood supply*; D014655:Vascular Resistance
chemical_list: C064980:GH2 protein, human; D010926:Placental Hormones; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone