Abstract
Eicosanoids have been implicated in the adaptation of the fetal to the neonatal circulation, but biochemical support for an activation of their synthesis in relation to birth has not been presented. We addressed this by assessing in pairs the excretion of two metabolites of thromboxane A 2, 11-dehydro-TxB 2 (dTx) and 2,3-dinor-TxB 2 (Tx-M), and one metabolite of prostacyclin, 2,3-dinor-6-keto-PGF 1 a (PGI-M), in the first voided urine from 13 healthy term neonates and in the immediate pre-delivery urine from their respective mothers. The excretion of dTx was higher (p<0.01) in the neonates than in their mothers (7430 and 1330 pg/mg creatinine, respectively), and so was the excretion of Tx-M (3730 and 900 pg/mg creatinine, respectively, p<0.001). Also the excretion of PGI-M was higher (p<0.05) in the neonates than in their mothers (2550 vs 1510 pg/mg creatinine). Amniotic fluid contained detectable levels of both Tx-M and PGI-M. These data indicate that activation of platelets takes place in the neonate after separation of the fetal and maternal vascular circuits. The possible physiological implications of such activation requires further studies.
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