These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Lack of association between Doppler velocimetry and synthesis of prostacyclin and thromboxane in umbilical cord vessels from growth retarded fetuses. Author: Saldeen P, Olofsson P, Marsál K. Journal: Acta Obstet Gynecol Scand; 1995 Feb; 74(2):103-8. PubMed ID: 7900504. 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. CONCLUSION: 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.[Abstract] [Full Text] [Related] [New Search]