2-3-dinor-6-ketoprostaglandin-f1alpha and Asphyxia-Neonatorum

Decreased fetoplacental prostacyclin (PGI2) production has been shown in preeclampsia, and increased pulmonary PGI2 synthesis has been demonstrated in experimental hypoxia. We measured the urinary excretion of the main metabolites of PGI2, 6-keto-prostaglandin F1 alpha (6-keto) and 2,3-dinor-6-keto-prostaglandin F1 alpha (2,3-dinor), during the first day of life in infants born to mothers with preeclampsia (n = 26), in infants with birth asphyxia (n = 12), and in control infants (n = 14). The mean excretion of 6-keto in control infants increased from 9.3 to 14.3 ng/h/1.73 m2 from 0-12 to 12-24 h of age, and a corresponding change from 3.5 to 7.0 ng/h/1.73 m2 was seen in 2,3-dinor excretion. In infants of preeclamptic mothers the excretion values at 0-12 and 12-24 h and the pattern of change were not significantly different from controls. In asphyxiated infants, the mean excretion values at 0-12 and 12-24 h of 6-keto (11.0 and 11.6 ng/h/1.73 m2) and 2,3-dinor (6.0 and 5.8 ng/h/1.73 m2) were not significantly different from control infants, but no increase was seen. We conclude that PGI2 production in infants of preeclamptic mothers is not impaired, but after perinatal asphyxia there is an altered pattern of PGI2 metabolite excretion, suggesting decreased production capacity.

Topics: 6-Ketoprostaglandin F1 alpha; Asphyxia Neonatorum; Creatinine; Epoprostenol; Female; Humans; Infant, Newborn; Kidney; Male; Pre-Eclampsia; Pregnancy