Early inhaled nitric oxide at high dose enhances rat lung development after birth

Duong‐Quy, Sy; Hua-Huy, T.; Pham, Hoa; Tang, Xin; Jc, Mercier; Baud, Olivier; Dinh-Xuan, Anh Tuan

doi:10.1016/j.niox.2014.02.004

Cited by 12 publications

(10 citation statements)

References 48 publications

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“…In addition, our results showed an increase of SOD activity in the lungs of rat pups treated with iNO (figure 5). The increased SOD activity is in accordance with our previous results that iNO treatment even at the high dose of 20 ppm did not enhance oxidative stress as evaluated by 3-nitrotyrosine expression [2]. In fact, in some pathological conditions such as cigarette smoke exposure and acute lung injury, constitutive NOS activity is affected and inducible NOS is stimulated, leading to increased reactive oxygen species formation, and the SOD enzymes are nitrated and inactivated.…”

Section: Discussionsupporting

confidence: 91%

“…Protein extraction from frozen lung samples was performed as previously described [2]. For Western blots, equal amounts of pulmonary homogenates (50 µg per animal) were subjected to 7.5% SDS-PAGE and then transferred to polyvinylidene difluoride membranes (Immobilon-P; Millipore, Molsheim, France).…”

Section: Methodsmentioning

confidence: 99%

“…In our previous study, iNO enhanced rat lung development at early post-natal life, probably through increased expression of haem oxygenase-1, vascular endothelial growth factor and matrix metallopeptidase-2 pathways in full-term rat pups [2]. The present study aimed to assess the effects of iNO at low dose (5 ppm) or high dose (20 ppm) on the activity and expression of eNOS in newborn rat lungs.…”

Section: Introductionmentioning

confidence: 95%

“…NO is a selective pulmonary vasodilator, capable of reducing pulmonary vascular resistance and inhibiting vascular remodelling. In animal models, iNO has been found to promote angiogenesis, decrease apoptosis, and enhance surfactant function and alveolar formation [1, 2]. Notwithstanding these theoretical beneficial effects, recent clinical trials found that iNO does not reduce morbidity of bronchopulmonary dysplasia in pre-term infants [3, 4].…”

Section: Introductionmentioning

confidence: 99%

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Inhaled nitric oxide decreases pulmonary endothelial nitric oxide synthase expression and activity in normal newborn rat lungs

et al. 2016

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Inhaled nitric oxide (iNO) is commonly used in the treatment of very ill pre-term newborns. Previous studies showed that exogenous NO could affect endothelial NO synthase (eNOS) activity and expression in vascular endothelial cell cultures or adult rat models, but this has never been fully described in newborn rat lungs. We therefore aimed to assess the effects of iNO on eNOS expression and activity in newborn rats.Rat pups, post-natal day (P) 0 to P7, and their dams were placed in a chamber containing NO at 5 ppm (iNO-5 ppm group) or 20 ppm (iNO-20 ppm group), or in room air (control group). Rat pups were sacrificed at P7 and P14 for evaluation of lung eNOS expression and activity.At P7, eNOS protein expression in total lung lysates, in bronchial and arterial sections, was significantly decreased in the iNO-20 ppm versus control group. At P14, eNOS expression was comparable among all three groups. The amounts of eNOS mRNA significantly differed at P7 between the iNO-20 ppm and control groups. NOS activity decreased in the iNO-20 ppm group at P7 and returned to normal levels at P14. There was an imbalance between superoxide dismutase and NOS activities in the iNO-20 ppm group at P7.Inhalation of NO at 20 ppm early after birth decreases eNOS gene transcription, protein expression and enzyme activity. This decrease might account for the rebound phenomenon observed in patients treated with iNO.

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Section: Discussionsupporting

confidence: 91%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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Inhaled nitric oxide decreases pulmonary endothelial nitric oxide synthase expression and activity in normal newborn rat lungs

et al. 2016

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“…One recent report has indicated that treatment of newborn rats with highdose (20 ppm) inhaled NO improved lung growth, most likely through increased expression of hemeoxygenase-1 and VEGF/ VEGF receptor 2 (VEGFR2), as well as matrix metalloproteinases (MMPs). Interestingly, increased gene expression was seen over the course of NO administration but was lost after discontinuation of NO (89). The immediate implication of this study is not clear because NO administration was made in room air to healthy, properly developing rat lungs.…”

Section: New Mediators and Modulators Of Impaired Alveolarizationmentioning

confidence: 83%

Recent advances in the mechanisms of lung alveolarization and the pathogenesis of bronchopulmonary dysplasia

Silva

Nardiello

Pozarska

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

120

117

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Alveolarization is the process by which the alveoli, the principal gas exchange units of the lung, are formed. Along with the maturation of the pulmonary vasculature, alveolarization is the objective of late lung development. The terminal airspaces that were formed during early lung development are divided by the process of secondary septation, progressively generating an increasing number of alveoli that are of smaller size, which substantially increases the surface area over which gas exchange can take place. Disturbances to alveolarization occur in bronchopulmonary dysplasia (BPD), which can be complicated by perturbations to the pulmonary vasculature that are associated with the development of pulmonary hypertension. Disturbances to lung development may also occur in persistent pulmonary hypertension of the newborn in term newborn infants, as well as in patients with congenital diaphragmatic hernia. These disturbances can lead to the formation of lungs with fewer and larger alveoli and a dysmorphic pulmonary vasculature. Consequently, affected lungs exhibit a reduced capacity for gas exchange, with important implications for morbidity and mortality in the immediate postnatal period and respiratory health consequences that may persist into adulthood. It is the objective of this Perspectives article to update the reader about recent developments in our understanding of the molecular mechanisms of alveolarization and the pathogenesis of BPD.

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Effects of Hyperoxia on the Developing Airway and Pulmonary Vasculature

Pabelick

Thompson

Britt

2017

Advances in Experimental Medicine and Biology

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Although it is necessary and part of standard practice, supplemental oxygen (40-90% O) or hyperoxia is a significant contributing factor to development of bronchopulmonary dysplasia, persistent pulmonary hypertension, recurrent wheezing, and asthma in preterm infants. This chapter discusses hyperoxia and the role of redox signaling in the context of neonatal lung growth and disease. Here, we discuss how hyperoxia promotes dysfunction in the airway and the known redox-mediated mechanisms that are important for postnatal vascular and alveolar development. Whether in the airway or alveoli, redox pathways are important and greatly influence the neonatal lung.

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Early inhaled nitric oxide at high dose enhances rat lung development after birth

Cited by 12 publications

References 48 publications

Inhaled nitric oxide decreases pulmonary endothelial nitric oxide synthase expression and activity in normal newborn rat lungs

Inhaled nitric oxide decreases pulmonary endothelial nitric oxide synthase expression and activity in normal newborn rat lungs

Recent advances in the mechanisms of lung alveolarization and the pathogenesis of bronchopulmonary dysplasia

Effects of Hyperoxia on the Developing Airway and Pulmonary Vasculature

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