Inhaled Nitric Oxide for Preterm Neonates

Arul, Nandini; Konduri, Girija G.

doi:10.1016/j.clp.2008.09.002

Cited by 15 publications

(13 citation statements)

References 92 publications

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“…Thus, it remains unclear why in our studies adding iNO to the RA exposure increased alveolar number and decreased neutrophil influx in the lung. Furthermore, NO in the presence of hyperoxia can be metabolized to compounds that can exert either pro-oxidant or anti-oxidant effects (22,23). It may be that there is an advantage to adding iNO to room air, since we found a positive effect on lung growth and there would be less chance for the production of pro-oxidant metabolites of NO, although clinical trials are necessary.…”

Section: Discussionmentioning

confidence: 99%

Inhaled Nitric Oxide Decreases Leukocyte Trafficking in the Neonatal Mouse Lung During Exposure to >95% Oxygen

et al. 2010

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Chronic lung injury in the neonate is termed bronchopulmonary dysplasia (BPD). These patients generally require supplemental oxygen therapy, and hyperoxia has been implicated in the pathogenesis of BPD. The concomitant use of oxygen and inhaled NO (iNO) may result in the generation of reactive nitrogen species or may have an anti-inflammatory effect in the neonatal lung. We tested the hypothesis that exposure to Ͼ95% O 2 in neonatal mice would increase trafficking of leukocytes into the lung and that the addition of iNO to Ͼ95% O 2 would decrease this leukocyte trafficking. Hyperoxia resulted in fewer alveoli, increased presence of neutrophils and macrophages, and decreased number of mast cells within the lung parenchyma. Adding iNO to hyperoxia prevented the hyperoxia-induced changes and resulted in the numbers of alveoli, neutrophils, macrophages, and mast cells approximating those found in controls (room air exposure). Intercellular adhesion molecule (ICAM) and monocyte chemotactic protein-1 (MCP-1), two factors responsible for leukocyte recruitment, were up-regulated by hyperoxic exposure, but the addition of iNO to the hyperoxic exposure prevented the hyperoxia-induced up-regulation of ICAM and MCP-1. These data demonstrate that iNO alters the hyperoxia-induced recruitment of leukocytes into the lung. (Pediatr Res 67: 244-249, 2010) E xposure to supplemental oxygen commonly results in the local production of proinflammatory cytokines, recruitment of leukocytes, and oxidative tissue injury (1-4). However, supplemental oxygen can be life saving in the intensive care unit setting. Hyperoxic exposure in the neonatal period is associated with arrested or delayed development of postnatal lung maturation (5). The specific mechanisms underlying hyperoxia-induced arrested lung development are not completely defined, although increased oxidative stress and activation of the inflammatory cascade, as well as infiltration of leukocytes into the lungs are recognized as important contributors. These factors are also thought to contribute to the pathogenesis of chronic neonatal lung diseases, such as bronchopulmonary dysplasia (BPD).Inhaled NO (iNO), a selective pulmonary vasodilator, has been used in term and near-term infants with pulmonary hypertension (6 -8). Recently, the clinical use of iNO for the prevention and/or treatment of BPD have been suggested (9). Supplemental O 2 therapy is commonly used in combination with iNO in the intensive care unit; however, their mechanistic and physiologic interactions in vivo are not completely understood. For example, in biologic settings NO is known to avidly interact with reactive oxygen species to generate reactive nitrogen species such as peroxynitrite, a potent oxidizing agent that can cause cellular injury and death. In contrast, iNO has also been shown to prevent tissue injury in the lung (9). Thus, the interplay between supplemental O 2 therapy and iNO may result in a wide range of physiologic effects, and furthermore, the net effect may be either beneficial or ...

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Section: Discussionmentioning

confidence: 99%

Inhaled Nitric Oxide Decreases Leukocyte Trafficking in the Neonatal Mouse Lung During Exposure to >95% Oxygen

et al. 2010

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“…179 Here we briefly discuss the anti-inflammatory properties of NO. 180,181 Many of its anti-inflammatory properties are mediated through the inhibition of canonical, inflammatory stress-induced, and atypical, oxidant stress-induced NF-B activation. 44,[182][183][184][185][186][187][188][189][190][191][192][193] This is seen in healthy adult human subjects who have a higher endogenous NO production and associated NF-B inhibition when compared with asthmatic subjects and those with pulmonary hypertension.…”

Section: No and Its Role As An Antiinflammatory Agentmentioning

confidence: 99%

Targeting Inflammation to Prevent Bronchopulmonary Dysplasia: Can New Insights Be Translated Into Therapies?

2011

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Bronchopulmonary dysplasia (BPD) frequently complicates preterm birth and leads to significant long-term morbidity. Unfortunately, few therapies are known to effectively prevent or treat BPD. Ongoing research has been focusing on potential therapies to limit inflammation in the preterm lung. In this review we highlight recent bench and clinical research aimed at understanding the role of inflammation in the pathogenesis of BPD. We also critically assess currently used therapies and promising developments in the field.

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“…Inhaled nitric oxide (iNO; INOmax ® , INO Therapeutics, Hampton, NJ, USA) selectively dilates the pulmonary vasculature, rapidly diffuses across the alveolar-capillary membrane, and binds to hemoglobin with minimal systemic effects [1,2]. In pivotal studies of late preterm and term neonates with hypoxic respiratory failure (HRF) and pulmonary hypertension (PH), iNO therapy has been shown to improve oxygenation and reduce the need for extracorporeal membrane oxygenation [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Efficacy of inhaled nitric oxide in neonates with hypoxic respiratory failure and pulmonary hypertension: the Japanese experience

Suzuki

Togari

Potenziano

et al. 2018

Journal of Perinatal Medicine

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Objective: To analyze data from a registry of Japanese neonates with hypoxic respiratory failure associated with pulmonary hypertension (PH) to compare the effectiveness of inhaled nitric oxide (iNO) in neonates born <34 weeks vs. ≥34 weeks gestational age (GA). Materials and methods: iNO was administered according to approved Japanese product labeling. Study data were collected before iNO administration and at predefined intervals until discontinuation. Results: A total of 1,114 neonates were included (n = 431, <34 weeks GA; n = 675, ≥34 weeks GA; n = 8, missing age data). Mean decrease from baseline oxygenation index (OI) was similar in both age groups. OI reduction was more pronounced in the <34 weeks subgroups with baseline OI ≥25. Survival rates were similar in the <34 weeks GA and ≥34 weeks GA groups stratified by baseline OI (OI < 15, 89% vs. 93%; 15 ≤ OI < 25, 85% vs. 91%; 25 ≤ OI ≤ 40, 73% vs. 79%; OI > 40, 64% vs. 66%). Conclusion: iNO improved oxygenation in preterm neonates as effectively as in late preterm and term neonates, without negative impact on survival. If clinically significant PH is present, as measured by pulse oximetry or echocardiography, a therapeutic trial of iNO might be indicated for preterm neonates.

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Inhaled Nitric Oxide for Preterm Neonates

Cited by 15 publications

References 92 publications

Inhaled Nitric Oxide Decreases Leukocyte Trafficking in the Neonatal Mouse Lung During Exposure to >95% Oxygen

Inhaled Nitric Oxide Decreases Leukocyte Trafficking in the Neonatal Mouse Lung During Exposure to >95% Oxygen

Targeting Inflammation to Prevent Bronchopulmonary Dysplasia: Can New Insights Be Translated Into Therapies?

Efficacy of inhaled nitric oxide in neonates with hypoxic respiratory failure and pulmonary hypertension: the Japanese experience

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