Fetal anaemia and its relation with increased concentrations of adenosine.

Abstract

Adenosine concentrations were measured in umbilical venous blood obtained by cordocentesis from 14 fetuses of 19-34 weeks' gestation. The concentration did not change significantly with gestational age, but anaemic fetuses showed significantly increased concentrations of adenosine and there was a positive association with blood oxygen tension. These findings suggest that the fetus responds to tissue hypoxia by increasing blood adenosine concentrations from at least 19 weeks' gestation. (Arch Dis Child 1993;68:35-6) Postnatal studies of infants who had been subjected to perinatal asphyxia have reported increased concentrations of catecholamines,' adenosine, and hypoxanthine in blood samples.2 5 Cordocentesis, ultrasound guided umbilical venous blood sampling, has now made it possible to investigate the metabolic consequences of intrauterine hypoxia. Previous work, using cordocentesis samples from rhesus isoimmunised fetuses, showed the presence of hypoxaemia and anaemia, and showed that these abnormalities were associated with increased concentrations of catecholamines.6The aim of this study was to measure adenosine concentrations in fetuses and determine their relation with prenatal hypoxia.

Changes in Plasma Adenosine Concentrations during Normal Pregnancy

“…A previous study demonstrated that the plasma [ADO] increases in anemic patients [8]. In this study, a slight decrease of the RBC count, hematocrit and hemoglobin concentration was observed.…”

Purinergic Signaling and Blood Vessels in Health and Disease

“…LPS upregulates ecto-59-nucleotidase activity on HUVECs, and it was suggested that because adenosine is an anti-inflammatory molecule, 59-nucleotidase upregulation may protect endothelial cells against inflammatory damage (Li et al, 2008b). Adenosine concentration in umbilical venous blood increased significantly in anemic fetuses, suggesting that the fetus responds to hypoxia by increasing blood adenosine (Ross Russell et al, 1993). Functional A 1 and A 2B receptors were shown to be expressed on the HUVEC-derived ECV304 cell line .…”

Hypoxia is an effective stimulus for vesicular release of ATP from human umbilical vein endothelial cells

“…Adenosine and ATP have also been implicated. Adenosine is released from the placenta into umbilical venous blood in anemia, hypoxia, growth retardation and pre-eclampsia [4–6] . Moreover, hypoxia decreases adenosine uptake via its endonucleoside transporter (ENT-1) in human umbilical vein endothelial cells (HUVEC) [6] .…”

“…Further, the balance of ATP, ADP and adenosine regulate platelet aggregation, inflammation, immunity, and vascular proliferation, high concentrations of ATP being pro-inflammatory and immunostimulatory [5,10–12] . It has been reported that ATP is released from endothelial cells by hypoxia [1,4,5] . However, whilst hypoxia augmented shear stress-stimulated ATP release from primary HUVEC, hypoxia alone did not affect ATP release [13] .…”