Decreased sodium ion absorption across nasal epithelium of very premature infants with respiratory distress syndrome,☆☆,,★★

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Abstract

Objective and study design: Successful adaptation to air breathing at birth depends on rapid absorption of fetal lung liquid that is mediated by activation of amiloride-sensitive sodium ion channels. To test the relationship between respiratory epithelial Na + transport and development of respiratory distress syndrome (RDS), we measured nasal transepithelial potential difference (PD) in 31 very premature (≤30 weeks of gestation) newborn infants. Infants were retrospectively assigned to RDS (22 infants) and non-RDS (9 infants) groups on the basis of clinical and chest x-ray criteria.

Results: Maximal nasal epithelial PD increased with birth weight (−1.2 mV/100 gm) and was lower in infants with RDS (−16.5 ± 0.6 mV) than in those without RDS (−22.0 ± 1.3 mV). Infants without RDS had PD values similar to normal fullterm infants. Amiloride inhibition of PD, an index of Na + absorption,, was significantly lower, within the first 24 hours of life, in infants in whom RDS developed (3.8 ± 0.2 mV; 29.5% ± 0.8% inhibition) than in those without RDS (6.1 ± 0.6 mV; 38.6% ± 0.5% inhibition). Maximal and amiloride-sensitive PD returned to normal during the recovery phase of RDS.

Conclusions: We conclude that Na + absorption across nasal epithelium increases with increasing birth weight and that impairment of Na + absorption across the respiratory epithelia of very premature infants may contribute to the pathogenesis of RDS.

Section snippets

METHODS

Our patient population consisted of 31 infants born at 30 weeks of gestation or less. We focused on infants born at that stage of gestation because the incidence of, and mortality rate from, RDS continues to be high in these infants. Infants were retrospectively assigned to an RDS group (22 infants) or a non-RDS group (9 infants). RDS was defined as respiratory distress associated with hypoxia, the need for mechanical ventilation for longer than 24 hours, and chest x-ray findings that were

RESULTS

Infants in the RDS and non-RDS groups were matched for gestational age (27.9 ± 0.4 weeks, non-RDS group; 27.2 ± 0.3 weeks, RDS group), but the mean birth weight of the non-RDS group (1101 ± 52 gm) was significantly higher than that of the RDS group (935 ± 44 gm; p <0.05). There was a tendency for Apgar scores to be lower in the RDS group (1-minute score: non-RDS group, 4.5 ± 0.8; RDS group, 3.6 ± 0.4; 5-minute score: non-RDS group, 7.4 ± 0.5; RDS group, 6.3 ± 0.3; p >0.05 at 1 and 5 minutes).

DISCUSSION

The principal cause of RDS is thought to be deficient surfactant production and secretion in the lungs of preterm infants. Widespread use of surfactant has decreased the morbidity and mortality rates associated with this disease. 16 However, RDS continues to be a significant cause of death in very premature infants, and the incidence of bronchopulmonary dysplasia has not decreased since the introduction of surfactant replacement therapy. 16 These observations suggest that surfactant deficiency

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    Two of the most common respiratory disorders in the human newborn, neonatal respiratory distress syndrome (RDS) and transient tachypnea of the newborn (TTN) have been associated with changes in the respiratory epithelium gene expression of the aquaporine-5 (AQP5) and the β subunit of the epithelial sodium channel (β-ENaC). RDS, which affects mainly premature infants, is characterized by a relative surfactant deficiency superimposed on an inability to adequately absorb fetal lung liquid [1, 11]; a decrease in the expression of β-ENaC has been strongly associated with this entity [7, 8, 9, 10]. TTN is triggered mainly by the delay of fetal lung liquid clearance [5, 7], it is more common in late-preterm and early-term newborns; and has been associated with an increment of the expression levels of AQP5 in tracheal aspirates [5, 7, 8, 9, 10].

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From the Department of Pediatrics and Medicine, University of North Carolina at Chapel Hill, and the Department of Pediatrics, University of Eastern Virginia and Hospital of the Kings Daughters, Norfolk, Virginia.

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Supported by the Cystic Fibrosis Foundation.

Reprint requests: Pierre M. Barker, MBChB, Department of Pediatrics, University of North Carolina at Chapel Hill, 635 Burnett-Womack Building, Manning Drive, Chapel Hill NC 27599-7220.

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