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Antenatal Sildenafil Treatment Attenuates Pulmonary Hypertension in Experimental Congenital Diaphragmatic Hernia
Author(s) -
Christina Luong,
Juliana Rey-Perra,
Arul Vadivel,
G. A. Gilmour,
Yves Sauvé,
Debby P.Y. Koonen,
Don K. Walker,
Kathryn G. Todd,
Pierre Gressèns,
Zamaneh Kassiri,
Khurram Nadeem,
Beverly C. Morgan,
Farah Eaton,
Jason R.B. Dyck,
Stephen L. Archer,
Bernard Thébaud
Publication year - 2011
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.108.845909
Subject(s) - medicine , sildenafil , congenital diaphragmatic hernia , nitrofen , pulmonary hypertension , pulmonary artery , pulmonary hypoplasia , lung , right ventricular hypertrophy , nitric oxide , cardiology , fetus , cgmp specific phosphodiesterase type 5 , endocrinology , pregnancy , biology , genetics
Lung hypoplasia and persistent pulmonary hypertension of the newborn limit survival in congenital diaphragmatic hernia (CDH). Unlike other diseases resulting in persistent pulmonary hypertension of the newborn, infants with CDH are refractory to inhaled nitric oxide (NO). Nitric oxide mediates pulmonary vasodilatation at birth in part via cyclic GMP production. Phosphodiesterase type 5 (PDE5) limits the effects of NO by inactivation of cyclic GMP. Because of the limited success in postnatal management of CDH, we hypothesized that antenatal PDE5 inhibition would attenuate pulmonary artery remodeling in experimental nitrofen-induced CDH.

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