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Am. J. Respir. Crit. Care Med., Volume 164, Number 6, September 2001, 1083-1089

Restoring Effects of Vitamin A on Surfactant Synthesis in Nitrofen-induced Congenital Diaphragmatic Hernia in Rats

BERNARD THÉBAUD, ANNE-MARIE BARLIER-MUR, BERNADETTE CHAILLEY-HEU, ALEXANDRA HENRION-CAUDE, DICK TIBBOEL, ANH-TUAN DINH-XUAN, and JACQUES R. BOURBON

Réanimation Néonatale-UPRES 2704, Hôpital Antoine Béclère, Université Paris-Sud, Assistance Publique-Hôpitaux de Paris, Clamart; Service de Physiologie, Hôpital Cochin, Université René Descartes, Paris; INSERM, U3 19, Université Denis Diderot Paris-7, Paris, France; Pediatric Surgery, Sophia Children's Hospital, Rotterdam, The Netherlands

Congenital diaphragmatic hernia (CDH) is a major cause of refractory respiratory failure in the newborn. Besides pulmonary hypoplasia, the pathophysiology of CDH also includes surfactant deficiency. Vitamin A (vit A) is important for various aspects of lung development. We hypothesized that antenatal treatment with vit A would stimulate lung surfactant synthesis in experimental CDH induced in rats by maternal ingestion of the herbicide nitrofen (2,4-dichloro-phenyl-p-nitrophenyl-ether) on Day 12. Fetuses were assigned to six experimental groups: (1) controls from rats that received olive oil, the vehicle; (2) fetuses from rats that received olive oil on Day 12 and vit A orally (15,000 IU) on Day 14; (3) nitrofen (N)-exposed fetuses without diaphragmatic hernia (N/no DH); (4) N/no DH from rats given vit A on Day 14; (5 ) nitrofen-exposed fetuses with DH (N/+DH); (6) N/+DH from rats given vit A on Day 14. Fetuses were delivered by C-section at Day 21. Lung DNA content was lowered in the nitrofen group as compared with the controls group, but increased by subsequent vit A treatment. Lung surfactant disaturated phosphatidylcholine was reduced in the N/+DH group and restored to control level by vit A. The expression level of surfactant proteins (SP) -A and -C was decreased in vit A-treated control rats and in nitrofen-exposed fetuses with or without DH. Vit A restored SP-A and -C mRNA expression to control levels in N/+DH. SP-B expression was lowered in N/no DH and increased by vit A in this group. The proportion of type II cells assessed by SP-B immunolabeling was lowered in N/+DH and restored by vit A treatment. We conclude that antenatal treatment with vit A restores lung maturation in nitrofen-induced hypoplastic lungs with CDH. These findings point out vit A as a potential therapeutical agent for correcting surfactant deficiency in CDH.




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