The aim of this study was to investigate the possible mechanism of the regulation of plasma adenosine concentration [ADO] in normal pregnancy. We measured the activities of circulating enzymes that are involved in the production and metabolism of adenosine, and plasma [ADO] in nonpregnant (n = 14) and normal pregnant women (n = 14) in the third trimester. In pregnant women, the activity of plasma 5′-nucleotidase and plasma [ADO] were significantly elevated and plasma adenosine deaminase activity was significantly reduced. Enzymatic activities of both plasma enzymes appear to be changed in a way that would favor increased adenosine concentrations.
Adenosine is an established platelet activation suppressor. Increased plasma levels of adenosine in preeclampsia might partially compensate and tend to prevent further excessive platelet activation in women with preeclampsia.
The present study investigated serum adenosine deaminase (ADA) activity and the patterns of two ADA isoenzymes, ADA1 and ADA2, and to evaluate the possible role of cell-mediated immunity as causes of the changes in ADA activity in pre-eclampsia. We measured serum activities of total ADA, ADA1 and ADA2 in pre-eclampsia (n = 22) and normal pregnancy (n = 22). Peripheral blood monocyte counts and neopterin levels, reflecting the activation of the monocyte-macrophage cell system, were also measured. In pre-eclampsia, serum total ADA and ADA2 activities were significantly increased compared with normal pregnancy (p < 0.05), which were accompanied by increases in serum neopterin levels. These results suggest that increased total ADA activity reflects increases in ADA2 activity, which may be in part related to enhanced cell-mediated immunity during pre-eclampsia.
The aim of this study was to measure changes in plasma adenosine concentration [ADO] during a normal pregnancy and to evaluate the possible role of platelets and red blood cells (RBC) as causes of changes in plasma [ADO]. We measured the plasma [ADO] in normal pregnant women (n = 11) during the first, second and third trimesters. The mean plasma [ADO] in the third trimester was 0.41 ± 0.08 μM (means ± SEM), significantly higher than in the first and second trimesters (p < 0.05). In pregnant women, platelet and RBC counts, hematocrit and hemoglobin concentration decreased slightly throughout the pregnancy. The elevation in the plasma [ADO] correlated inversely with the platelet count (r = –0.43, p < 0.05). These results suggest that an increase in the plasma [ADO] in the third trimester may be attributed to the enhanced adenosine release from activated platelets.
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