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Am J Physiol Lung Cell Mol Physiol 278: L923-L932, 2000;
1040-0605/00 $5.00
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Vol. 278, Issue 5, L923-L932, May 2000

ETA-receptor blockade and ETB-receptor stimulation in experimental congenital diaphragmatic hernia

Bernard Thébaud1,2, Pascal de Lagausie1,3, Dominique Forgues4, Yves Aigrain3,5, Jean-Christophe Mercier6, and A. Tuan Dinh-Xuan1

2 Service de Réanimation Néonatale, Hôpital Antoine Béclère, Université Paris-Sud, 92140 Clamart; 1 Service de Physiologie-Explorations Fonctionnelles, Hôpital Cochin, Assistance Publique-Hôpitaux de Paris-Université Paris V, 75014 Paris; 3 Service de Chirurgie Viscérale Pédiatrique and 6 Service de Réanimation Pédiatrique, Hôpital Robert Debré, Assistance Publique-Hôpitaux de Paris-Université Paris VII, 75019 Paris; 5 Ecole de Chirurgie, Assistance Publique-Hôpitaux de Paris, 75005 Paris; and 4 Service de Chirurgie Viscérale Infantile, Centre Hospitalier Universitaire Montpellier, 34000 Montpellier, France

The aim of this study was to assess the role of nitric oxide (NO) and endothelin (ET)-1 in the pathophysiology of persistent pulmonary hypertension of the newborn in fetal lambs with a surgically created congenital diaphragmatic hernia (CDH). The pulmonary vascular response to various agonists and antagonists was assessed in vivo between 128 and 132 days gestation. Age-matched fetal lambs served as control animals. Control and CDH lambs had similar pulmonary vasodilator responses to acetylcholine, sodium nitroprusside, zaprinast, and dipyridamole. The ETA-receptor antagonist BQ-123 caused a significantly greater pulmonary vasodilatation in CDH than in control animals. The ETB-receptor agonist sarafotoxin 6c induced a biphasic response, with a sustained pulmonary vasoconstriction after a transient pulmonary vasodilatation that was not seen in CDH animals. We conclude that the NO signaling pathway in vivo is intact in experimental CDH. In contrast, ETA-receptor blockade and ETB-receptor stimulation significantly differed in CDH animals compared with control animals. Imbalance of ET-1-receptor activation favoring pulmonary vasoconstriction rather than altered NO-mediated pulmonary vasodilatation is likely to account for persistent pulmonary hypertension of the newborn in fetal lambs with a surgically created CDH.

persistent pulmonary hypertension of the newborn; nitric oxide; vascular endothelium


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