Increased plasma immunoreactive 6-keto-prostaglandin F1 alpha levels in newborns with idiopathic respiratory distress syndrome.

Serial plasma concentrations of immunoreactive 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), the stable hydration product of prostacyclin (PGI2), were measured with radioimmunoassay during the first month of life in 25 preterm infants with idiopathic respiratory distress syndrome (IRDS) and 38 preterm controls with normal heart and lung function. The levels of 6-keto-PGF1 alpha (521 +/- 81 pg/ml, mean +/- S.E.) in the infants with IRDS were higher (P less than 0.05) than those in the controls (335 +/- 42 pg/ml) on the first day of life, but thereafter no difference was seen. The highest first day 6-keto-PGF1 alpha level (1448 pg/ml) was found in the infant who died because of severe IRDS at the age of 19 h. The plasma 6-keto-PGF1 alpha concentrations in the distressed infants correlated positively with the alveolar-arterial oxygen gradient and the need of additional oxygen, but negatively with the arterial pH. In addition, an inverse correlation between the first day concentrations of 6-keto-PGF1 alpha and the lowest arterial oxygen tension in infants needing assisted ventilation was found. The mode of delivery (Cesarean section versus vaginal delivery) the gestational age, birth weight, sex or Apgar scores of the infants were not related to the 6-keto-PGF1 alpha levels on the first day of life. Neither did maternal pre-eclampsia, diabetes mellitus, or antenatal glucocorticoid treatment have any effect on the 6-keto-PGF1 alpha concentrations in the newborns. Our data suggest that a surge of the vasodilatory and antiaggregatory PGI2 is released during the early stage of IRDS, possibly in an attempt to increase the pulmonary perfusion. Our results give further indirect evidence that hypoxia stimulates the PGI2 production. High plasma immunoreactive 6-keto-PGF1 alpha levels during the early phase of IRDS suggest an increased generation of the vasodilatory and antiaggregatory PGI2 in this syndrome. This may be an attempt to overcome the increased pulmonary vasconstriction in IRDS. When the PGI2 formation rapidly declines after the first day of life, a relative PGI2 deficiency may ensue.