Urinary excretion rates of 6–keto–PGF 1α , in preterm infants recovering from respiratory distress with and without patent ductus arteriosus

Abstract

Patency of the ductus arteriosus in preterm infants is mediated by vasodilating prostanoids; however, reliable methods to monitor prostanoid activity or production in preterm infants are lacking. We measured the excretion rates of major and characteristic urinary metabolites of prostacyclin (PGI 2), PGE 1 and PGE 2, 6-keto-PGF 1α, and 7α-hydroxy-5,11-diketotetranorprostane-1,16-dioic acid (PGE-M), respectively. Besides these parameters which reflect total body prostanoid turnover and production, the urinary levels of PGE 2 and PGF 2α, the primary prostaglandins, were measured as an index of renal prostanoid synthesis. There were four study groups. One contained 11 thriving preterm infants; a second, six preterm infants with respiratory distress syndrome (RDS); a third, 30 preterm infants with RDS and patent ductus arteriosus (PDA); and a fourth, nine fullterm infants. All infants with RDS required artificial ventilation. There were no significant differences in PGE-M, PGE 2 and PGF 2α excretion rates among the various groups; however, a significant increase of the 6-keto-PGF 1α excretion rates was observed in the groups of infants with RDS and with and without PDA (P < 0.01 and P < 0.02, respectively). Spontaneous (n = 2) or indomethacin-induced (n = 6) closure of PDA was associated with weaning from the respirator and a concomitant drop into the normal and subnormal range of the excretion rates of 6-keto-PGF1, (P < 0.01) and PGE-M (P < 0.02). © International Pediatrics Research Foundation, Inc. 1984. All Rights Reserved.