Yoneyama Y, Sawa R, Suzuki S, Shin S, Power G G, Araki T
Department of Obstetrics and Gynecology, Nippon Medical School, Tokyo, Japan.
Am J Obstet Gynecol. 1996 Jan;174(1 Pt 1):267-71. doi: 10.1016/s0002-9378(96)70406-4.
The aim of this study was to evaluate the relationship between uteroplacental circulatory insufficiency and the fetoplacental release of adenosine in pregnancies complicated by preeclampsia.
We performed uterine artery Doppler velocimetry and calculated the pulsatility index of the uterine artery, to detect uteroplacental circulatory insufficiency, immediately before cordocentesis in 39 pregnant women complicated by preeclampsia. Umbilical venous blood obtained by cordocentesis was then analyzed for blood gases, pH, and plasma adenosine levels. Increased plasma adenosine was taken to signal its increased release from the placenta and fetus relative to its rate of disappearance.
The mean umbilical venous plasma adenosine level in the abnormal pulsatility index group was 1.78 +/- 0.17 mumol/L (mean +/- SEM, n = 25), significantly higher than in the normal pulsatility index group 0.58 +/- 0.14 mumol/L (n = 14, p < 0.001). Furthermore, in the abnormal pulsatility index group the elevation of plasma adenosine levels in the umbilical vein was found even in normoxic fetuses.
Fetal plasma adenosine increases before uteroplacental circulatory insufficiency becomes severe enough to cause generalized fetal hypoxemia. We postulate that enhanced adenosine formation in the fetus, umbilical cord vessels, and particularly the placenta may, at least in part, contribute to control and maintenance of placental blood flow.
