title: Myometrial and placental artery reactivity alone cannot explain reduced placental perfusion in pre-eclampsia and intrauterine growth restriction.
abstract: OBJECTIVE
  (1) To investigate a possible association between myometrial and placental artery vasoreactivity and perfusion at the basal and chorionic plates, respectively. (2) To confirm that myometrial arteries from women with pre-eclampsia and intrauterine growth restriction exhibit an attenuated endothelium-dependent vasodilatory response.
  
  
  METHODS
  Women with normal pregnancy, pre-eclampsia and intrauterine growth restriction had a magnetic resonance scan to assess placental perfusion using a technique called intravoxel incoherent motion. At delivery, myometrial and chorionic plate placental arteries were assessed on a wire myograph. Vessels were pre-constricted with the thromboxane mimetic U46619 and dilated with incremental doses of bradykinin.
  
  
  RESULTS
  Pre-constricted myometrial arteries from women with pre-eclampsia or intrauterine growth restriction exhibited an attenuated vasodilatory response to bradykinin, compared with normal pregnancy (P < 0.0001). Pre-constricted placental arteries exhibited a minimal vasodilatory response in all three groups of women (P = 0.10). Maximal constrictor and vasodilatory responses of myometrial arteries were not associated with the perfusing fraction at the basal plate. Maximal constrictor and vasodilatory responses of chorionic plate placental arteries were not associated with the perfusing fraction at the chorionic plate.
  
  
  CONCLUSIONS
  We confirm that myometrial arteries from women with pre-eclampsia or intrauterine growth restriction exhibit an attenuated endothelium-dependent vasodilatory response. Apart from vasoreactivity of small arteries, other factors may be involved in the control of placental perfusion.
authors.affiliation: The MRC Development Group, School of Human Development, University of Nottingham, Maternity Unit, City Hospital, UK.
authors.forename: Stephen S
authors.initials: SS
authors.lastname: Ong
authors.forename: Rachel J
authors.initials: RJ
authors.lastname: Moore
authors.forename: Averil Y
authors.initials: AY
authors.lastname: Warren
authors.forename: Ian P
authors.initials: IP
authors.lastname: Crocker
authors.forename: Jon
authors.initials: J
authors.lastname: Fulford
authors.forename: Damian J
authors.initials: DJ
authors.lastname: Tyler
authors.forename: Penny A
authors.initials: PA
authors.lastname: Gowland
authors.forename: Philip N
authors.initials: PN
authors.lastname: Baker
mesh_terms: D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid / Q000494:pharmacology; D000328:Adult; D000704:Analysis of Variance; D001158:Arteries / Q000502:physiology; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D009215:Myometrium / Q000098:blood supply*; D010920:Placenta / Q000098:blood supply*; D021041:Placental Circulation / Q000502:physiology; D011225:Pre-Eclampsia / Q000209:etiology / Q000503:physiopathology*; D011247:Pregnancy; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000502:physiology
chemical_list: D014662:Vasoconstrictor Agents; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid