Effect of Initial Nitric Oxide Concentration on Outcome in Infants with Persistent Pulmonary Hypertension of the Newborn

Neonatology ◽  
1999 ◽  
Vol 75 (4) ◽  
pp. 215-224 ◽  
Author(s):  
Karen S. Wood ◽  
Martin J. McCaffrey ◽  
Jocelyn C. Donovan ◽  
Alan D. Stiles ◽  
Carl L. Bose
Children ◽  
2021 ◽  
Vol 8 (5) ◽  
pp. 378
Author(s):  
Satyan Lakshminrusimha ◽  
Sylvia F. Gugino ◽  
Krishnamurthy Sekar ◽  
Stephen Wedgwood ◽  
Carmon Koenigsknecht ◽  
...  

Resuscitation with 21% O2 may not achieve target oxygenation in preterm infants and in neonates with persistent pulmonary hypertension of the newborn (PPHN). Inhaled nitric oxide (iNO) at birth can reduce pulmonary vascular resistance (PVR) and improve PaO2. We studied the effect of iNO on oxygenation and changes in PVR in preterm lambs with and without PPHN during resuscitation and stabilization at birth. Preterm lambs with and without PPHN (induced by antenatal ductal ligation) were delivered at 134 d gestation (term is 147–150 d). Lambs without PPHN were ventilated with 21% O2, titrated O2 to maintain target oxygenation or 21% O2 + iNO (20 ppm) at birth for 30 min. Preterm lambs with PPHN were ventilated with 50% O2, titrated O2 or 50% O2 + iNO. Resuscitation with 21% O2 in preterm lambs and 50%O2 in PPHN lambs did not achieve target oxygenation. Inhaled NO significantly decreased PVR in all lambs and increased PaO2 in preterm lambs ventilated with 21% O2 similar to that achieved by titrated O2 (41 ± 9% at 30 min). Inhaled NO increased PaO2 to 45 ± 13, 45 ± 20 and 76 ± 11 mmHg with 50% O2, titrated O2 up to 100% and 50% O2 + iNO, respectively, in PPHN lambs. We concluded that iNO at birth reduces PVR and FiO2 required to achieve target PaO2.


2020 ◽  
Vol 13 (2) ◽  
pp. 175-182
Author(s):  
R. Dadiz ◽  
J. Nair ◽  
C.T. D’Angio ◽  
R.M. Ryan ◽  
S. Lakshminrusimha

2003 ◽  
Vol 67 (6) ◽  
pp. 585-590 ◽  
Author(s):  
Jonathan B. Hanson ◽  
Paul T. Russell ◽  
Andy T.A. Chung ◽  
Claire S. Kaura ◽  
Samantha H. Kaura ◽  
...  

2001 ◽  
Vol 164 (5) ◽  
pp. 834-839 ◽  
Author(s):  
ROBIN H. STEINHORN ◽  
GEORGE ALBERT ◽  
DANIEL D. SWARTZ ◽  
JAMES A. RUSSELL ◽  
CAROLYN R. LEVINE ◽  
...  

2014 ◽  
Vol 173 (10) ◽  
pp. 1381-1385 ◽  
Author(s):  
Sema Tanriverdi ◽  
Ozge Altun Koroglu ◽  
Ozgun Uygur ◽  
Can Balkan ◽  
Mehmet Yalaz ◽  
...  

1995 ◽  
Vol 10 (6) ◽  
pp. 270-282
Author(s):  
Stella Kourembanas

Persistent pulmonary hypertension of the newborn (PPHN) is a common cause of respiratory failure in the full-term neonate. Molecular and cellular studies in vascular biology have revealed that endothelial-derived mediators play a critical role in the pathogenesis and treatment of PPHN. Endothelial-derived vasoconstrictors, like endothelin, may increase smooth muscle cell contractility and growth, leading to the physiologic and structural changes observed in the pulmonary arterioles of infants with this disease. On the other hand, decreased production of the endothelial-derived relaxing factor, nitric oxide, may exacerbate pulmonary vasoreactivity and lead to more severe pulmonary hypertension. Exogenous (inhaled) nitric oxide therapy reduces pulmonary vascular resistance and improves oxygenation. The safety and efficacy of this therapy in reducing the need for extracorporeal membrane oxygenation and decreasing long-term morbidity is being tested in several trials nationally and abroad. Understanding the basic mechanisms that regulate the gene expression and production of these vasoactive mediators will lead to improved preventive and therapeutic strategies for PPHN.


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