scholarly journals Persistent Pulmonary Hypertension of the Newborn: The Efficacy Comparison of Vasodilators Sildenafil Plus Bosentan Versus Sildenafil Plus Beraprost at a Tertiary Childcare Health Facility

Cureus ◽  
2021 ◽  
Author(s):  
Mudasser Adnan ◽  
Muhammad Sohail Arshad ◽  
Hafiz Muhammad Anwar-ul-Haq ◽  
Munir Ahmad ◽  
Hira Afsheen ◽  
...  
1997 ◽  
Vol 17 (6) ◽  
pp. 959-975 ◽  
Author(s):  
Sibylle Haraida ◽  
Hannelore Lochbuhler ◽  
A. Heger ◽  
A. Nerlich ◽  
J. Diebold ◽  
...  

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

1997 ◽  
Vol 105 (2) ◽  
pp. 202-206 ◽  
Author(s):  
C Bearer ◽  
R K Emerson ◽  
M A O'Riordan ◽  
E Roitman ◽  
C Shackleton

Author(s):  
George Lister

Persistent pulmonary hypertension of the newborn or persistent fetal circulation is a clinical syndrome that is usually apparent within the first 2 days after birth because of the presence of hypoxemia (2;12;19). The syndrome was first described in an abstract by Gersony, Due, and Sinclair (6) in 1969. Two infants were reported who had “RV decompensation, cyanosis and clear lung fields… in the absence of recognizable cardiac, pulmonary, hematologic or CNS disease.” The syndrome has been associated with aspiration of meconium, diaphragmatic hernia, asphyxia, hemorrhage, shock, and maternal infection (4;18). In other cases, there is no clear antecedent event. Despite considerable interest in the problem and a wealth of research related to pulmonary vasoregulation and vascular development in the fetus and newborn, the etiology of the syndrome remains obscure 20 years since its recognition.


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