Abstract

Increased pulmonary vascular resistance in preterm newborn infants with respiratory distress syndrome is suggested, and endothelin-1 plays an important role in pulmonary vascular reactivity in newborns. We determined umbilical cord blood and neonatal (second sample) levels of endothelin-1 in 18 preterm newborns with respiratory distress syndrome who had no clinical or echocardiographic diagnosis of pulmonary hypertension and 22 without respiratory distress syndrome (gestational ages: 31.4 +/- 1.6 and 29.3 +/- 2.3 weeks, respectively). Umbilical cord blood and a second blood sample taken 18 to 40 h after birth were used for endothelin-1 determination by enzyme immunoassay. Median umbilical cord blood endothelin-1 levels were similar in both groups (control: 10.9 and respiratory distress syndrome: 11.4 pg/mL) and were significantly higher than in the second sample (control: 1.7 pg/mL and respiratory distress syndrome: 3.5 pg/mL, P < 0.001 for both groups). Median endothelin-1 levels in the second sample were significantly higher in children with respiratory distress syndrome than in control infants (P < 0.001). There were significant positive correlations between second sample endothelin-1 and Score for Neonatal Acute Physiology and Perinatal Extension II (r = 0.36, P = 0.02), and duration of mechanical ventilation (r = 0.64, P = 0.02). A slower decline of endothelin-1 from birth to 40 h of life was observed in newborns with respiratory distress syndrome when compared to controls. A significant correlation between neonatal endothelin-1 levels and some illness-severity signs suggests that endothelin-1 plays a role in the natural course of respiratory distress syndrome in preterm newborns.

Highlights

  • Recent studies suggest that there is increased pulmonary vascular resistance in preterm newborn infants with respiratory distress syndrome (RDS)

  • Median umbilical cord blood endothelin-1 levels were similar in both groups and were significantly higher than in the second sample

  • High blood ET-1 levels have been reported in neonatal sepsis [16], perinatal asphyxia [17,18], congenital diaphragmatic hernia [19], persistent pulmonary hypertension of the newborn [13,20,21,22,23], and acute respiratory distress syndrome (ARDS) in children [24]

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Summary

Introduction

Recent studies suggest that there is increased pulmonary vascular resistance in preterm newborn infants with respiratory distress syndrome (RDS). ET causes isolated contraction of pulmonary veins, vascular smooth muscle mitogenesis, myocardial cell hypertrophy, positive inotropic and chronotropic effects, bronchoconstriction, mucous secretion, cellular proliferation, and inflammatory reactions [511]. Experimental studies have suggested that ET-1 plays an important role in pulmonary vascular reactivity in neonatal RDS [3,14]. High blood ET-1 levels have been reported in neonatal sepsis [16], perinatal asphyxia [17,18], congenital diaphragmatic hernia [19], persistent pulmonary hypertension of the newborn [13,20,21,22,23], and acute respiratory distress syndrome (ARDS) in children [24]

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