LACK OF ASSOCIATION BETWEEN DOPPLER VELOCIMETRY AND SYNTHESIS OF PROSTACYCLIN AND THROMBOXANE IN UMBILICAL-CORD VESSELS FROM GROWTH-RETARDED FETUSES

Citation
P. Saldeen et al., LACK OF ASSOCIATION BETWEEN DOPPLER VELOCIMETRY AND SYNTHESIS OF PROSTACYCLIN AND THROMBOXANE IN UMBILICAL-CORD VESSELS FROM GROWTH-RETARDED FETUSES, Acta obstetricia et gynecologica Scandinavica, 74(2), 1995, pp. 103-108
Citations number
35
Categorie Soggetti
Obsetric & Gynecology
ISSN journal
00016349
Volume
74
Issue
2
Year of publication
1995
Pages
103 - 108
Database
ISI
SICI code
0001-6349(1995)74:2<103:LOABDV>2.0.ZU;2-S
Abstract
Background. The aim of this study was to investigate the possible asso ciation between Doppler velocimetry and synthesis of prostacyclin (PGI (2)) and thromboxane A(2) (TxA(2)) in umbilical cord vessels. The hypo thesis was that an altered balance between PGI(2) and TxA(2) productio n is associated with a change of artery flow resistance. Methods. 17 c ases 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-W hitney U test and simple linear regression were used for statistical a nalyses. Results. The umbilical vessel synthesis of both PGI(2) and Tx A(2) was in general lower in small-for-gestational age (SGA) cases (n= 10) compared to appropriate-for-gestational age (AGA) (n=28). In the v ein, the PGI(2)/TxA(2) ratio was significantly lower in SGA cases. No certain correlations were found between umbilical artery PI and venous velocity, respectively, and PGI(2) or TxA(2), or their ratio. Conclus ion. The prostanoid synthesis was in general lower in SGA cases, resul ting in a significantly lower PGI(2)/TxA(2) ratio in the umbilical vei n. This indicates that fetal growth retardation might be associated wi th a disturbed endothelial function in this vessel. The synthesis of P GI(2) and TxA(2) in the juxtaplacental umbilical cord vessels was not correlated to the umbilical artery PI or venous flow velocity It is po ssible that an altered release of prostanoids in the placental vascula ture and tissue accounts for the rise of umbilical artery flow resista nce instead.