CLOSURE OF PATENT DUCTUS-ARTERIOSUS DECREASES PULMONARY MYELOPEROXIDASE IN PREMATURE-INFANTS WITH RESPIRATORY-DISTRESS SYNDROME

The aim of the study was to determine whether in premature infants wit h respiratory distress syndrome (RDS), an interrelationship existed be tween patent ductus arteriosus (PDA) and pulmonary neutrophil content. Thirteen premature infants with PDA (gestational age 26.9 +/- 2.4 wee ks, birth weight 903 +/- 300 g) were pair-matched with infants without PDA (gestations age 27.1 +/- 2.5 weeks, birth weight 1,041 +/- 430 g) with regard to gestational age, birth weight and severity of RDS. The myeloperoxidase (MPO) contents of tracheal aspirates were analyzed be fore (age 2.8 +/- 1.7 days, MPO I) and after closure of PDA with indom ethacin (5.5 +/- 1.9 days, MPO II), and at corresponding time points i n controls (2.6 +/- 1.6 and 4.8 +/- 1.8 days). In PDA patients closure of PDA decreased MPO from 14.7 (range 2.1-27.4) to 4.6 (1.2-8.0) mu g /mg protein (p = 0.0008), whereas in controls it remained unchanged: 5 .4 (2.9-7.8) and 5.3 (2.9-7.8; p = 0.58). A significant difference exi sted in the change in MPO contents between the infants with PDA and th e controls. In premature infants with RDS, closure of PDA decreases th e neutrophil content of the lungs. The effect may be caused by closure of PDA as such, or by indomethacin. The high pulmonary neutrophil con tent in PDA may exacerbate inflammatory processes and contribute to th e development of chronic pulmonary disease.