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Decreased sodium ion absorption across nasal epithelium of very premature infants with respiratory distress syndrome
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 respirator...
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Published in: | The Journal of pediatrics 1997-03, Vol.130 (3), p.373-377 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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. |
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ISSN: | 0022-3476 1097-6833 |
DOI: | 10.1016/S0022-3476(97)70198-7 |