Urinary Excretion of Prostacyclin Metabolites in Infants Born after Maternal Preeclampsia or with Birth Asphyxia

Abstract

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 F_1α (6-keto) and 2,3-dinor-6-keto-prostaglandin F_1α (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.