title: Lack of association between Doppler velocimetry and synthesis of prostacyclin and thromboxane in umbilical cord vessels from growth retarded fetuses.
abstract: BACKGROUND
  The aim of this study was to investigate the possible association between Doppler velocimetry and synthesis of prostacyclin (PGI2) and thromboxane A2 (TxA2) in umbilical cord vessels. The hypothesis was that an altered balance between PGI2 and TxA2 production is associated with a change of artery flow resistance.
  
  
  METHODS
  17 cases with a suspicion of intrauterine growth retardation and 21 normal pregnancies were studied. The umbilical artery pulsatility index (PI) and venous mean velocity were recorded in vivo by Doppler velocimetry. Cord vessel prostanoid synthesis was determined in vitro. The Mann-Whitney U test and simple linear regression were used for statistical analyses.
  
  
  RESULTS
  The umbilical vessel synthesis of both PGI2 and TxA2 was in general lower in small-for-gestational age (SGA) cases (n = 10) compared to appropriate-for-gestational age (AGA) (n = 28). In the vein, the PGI2/TxA2 ratio was significantly lower in SGA cases. No certain correlations were found between umbilical artery PI and venous velocity, respectively, and PGI2 or TxA2, or their ratio.
  
  
  CONCLUSIONS
  The prostanoid synthesis was in general lower in SGA cases, resulting in a significantly lower PGI2/TxA2 ratio in the umbilical vein. This indicates that fetal growth retardation might be associated with a disturbed endothelial function in this vessel. The synthesis of PGI2 and TxA2 in the juxtaplacental umbilical cord vessels was not correlated to the umbilical artery PI or venous flow velocity. It is possible that an altered release of prostanoids in the placental vasculature and tissue accounts for the rise of umbilical artery flow resistance instead.
authors.affiliation: Department of Obstetrics and Gynecology, University of Lund, Malmö General Hospital, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Saldeen
authors.forename: P
authors.initials: P
authors.lastname: Olofsson
authors.forename: K
authors.initials: K
authors.lastname: Marsál
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis / Q000097:blood; D001783:Blood Flow Velocity; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D011464:Epoprostenol / Q000096:biosynthesis* / Q000097:blood; D005260:Female; D005312:Fetal Blood / Q000378:metabolism*; D005317:Fetal Growth Retardation / Q000097:blood* / Q000000981:diagnostic imaging* / Q000503:physiopathology; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D011247:Pregnancy; D011673:Pulsatile Flow; D015203:Reproducibility of Results; D012212:Rheology; D013928:Thromboxane A2 / Q000096:biosynthesis* / Q000097:blood; D013929:Thromboxane B2 / Q000096:biosynthesis / Q000097:blood; D018617:Ultrasonography, Doppler, Pulsed; D016216:Ultrasonography, Prenatal; D014469:Umbilical Arteries / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D014471:Umbilical Veins / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology
chemical_list: D013929:Thromboxane B2; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol