Characterization Of In Vivo Fetal Intra-Airway Pressures In The Lamb Model Of Congenital Diaphragmatic Hernia

Author(s):  
Samuel C. Schecter ◽  
Mozziyar Etemadi ◽  
James A. Heller ◽  
Eveline Shue ◽  
William T. Ferrier ◽  
...  
2015 ◽  
Vol 35 (11) ◽  
pp. 1048-1056 ◽  
Author(s):  
Katika Nawapun ◽  
Mary Patrice Eastwood ◽  
Daysi Diaz-Cobos ◽  
Julio Jimenez ◽  
Michael Aertsen ◽  
...  

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 56A-56A
Author(s):  
Robert P Lemke ◽  
Grzegorz Sawicki ◽  
Cheung Po-Yin ◽  
Douglas W Allan ◽  
Richard Schulz ◽  
...  

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0209855
Author(s):  
Justin S. Baba ◽  
Timothy E. McKnight ◽  
M. Nance Ericson ◽  
Anthony Johnson ◽  
Kenneth J. Moise ◽  
...  

2005 ◽  
Vol 136A (1) ◽  
pp. 49-51 ◽  
Author(s):  
Osamu Shimokawa ◽  
Noriko Miyake ◽  
Takazumi Yoshimura ◽  
Nadiya Sosonkina ◽  
Naoki Harada ◽  
...  

2000 ◽  
Vol 278 (5) ◽  
pp. L923-L932 ◽  
Author(s):  
Bernard Thébaud ◽  
Pascal de Lagausie ◽  
Dominique Forgues ◽  
Yves Aigrain ◽  
Jean-Christophe Mercier ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document