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 with respiratory distress syndrome (RDS), an interrelationship existed between patent ductus arteriosus (PDA) and pulmonary neutrophil content. Thirteen premature infants with PDA (gestational age 26.9 +/- 2.4 weeks, 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 before (age 2.8 +/- 1.7 days, MPO I) and after closure of PDA with indomethacin (5.5 +/- 1.9 days, MPO II), and at corresponding time points in 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) micrograms/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 existed in the change in MPO contents between the infants with PDA and the controls. In premature infants with RDS, closure of PDA decreases the neutrophil content of the lungs. The effect may be caused by closure of PDA as such, or by indomethacin. The high pulmonary neutrophil content in PDA may exacerbate inflammatory processes and contribute to the development of chronic pulmonary disease.