Inhaled Nitric Oxide in Preterm Infants: A Systematic Review

Donohue, Pamela; Gilmore, Maureen; Cristofalo, Elizabeth; Wilson, Renée F; Weiner, Jonathan Z; Lau, Brandyn; Robinson, Karen A.; Allen, Marilee C

doi:10.1542/peds.2010-3428

Cited by 117 publications

(91 citation statements)

References 31 publications

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“…Систематические наблюдения и мета-анализ подтвердили эффективность использования NO для снижения смертности новорожденных [53]. NO часто применяют при лечении недоношенных детей для предотвращения развития бронхолегочной дисплазии [54,55]. Оксид азота оказался среди агентов с потен-циальным эпигенетическим эффектом, оказывающим свое действие на экспрессию генов через реакцию нитролизации [56].…”

Section: вопросы современной педиатрииunclassified

Premature Birth and Disease Programming. Contribution of Neonatal Intensive Care

Ковтун¹,

Цывьян²

2014

Vopr. sovr. pediatr.

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Section: вопросы современной педиатрииunclassified

Premature Birth and Disease Programming. Contribution of Neonatal Intensive Care

Ковтун¹,

Цывьян²

2014

Vopr. sovr. pediatr.

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Section: Nitric Oxidementioning

confidence: 99%

“…A recent case series indicates that iNO may reduce established BPDassociated pulmonary hypertension to a greater degree than oxygen alone [31]. On the other hand, large clinical trials have shown inconsistent benefit when iNO is used to prevent BPD [32][33][34][35].Outside of the NICU setting, the most common clinical use of iNO is for the infant or child with congenital heart disease with associated pulmonary hypertension. Postoperatively, iNO is frequently used to prevent or treat pulmonary hypertensive crises, improve oxygenation, and increase cardiac output.…”

mentioning

confidence: 99%

Pharmacotherapy of Pulmonary Hypertension

2013

Handbook of Experimental Pharmacology

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Pulmonary arterial hypertension is a serious disease with significant morbidity and mortality. While it can occur idiopathically, it is more commonly associated with other cardiac or lung diseases. While most of the available therapies were tested in adult populations, and most therapies in children remain off-label, new reports and randomized trials are emerging that inform the treatment of pediatric populations. This review discusses currently available therapies for pediatric pulmonary hypertension, their biologic rationales, and evidence for their clinical effectiveness. KeywordsPulmonary hypertension; Pulmonary vasculature; Vasodilator; Nitric Oxide; Phosphodiesterase; Prostacyclin; Endothelin NORMAL PULMONARY VASCULAR TRANSITIONDuring fetal life, the placenta serves as the organ of gas exchange, and the fetal circulation uses a series of adaptive mechanisms to maximize delivery of oxygen to metabolically active organs such as the brain, gut and kidney. The most highly oxygenated blood enters the fetus via the umbilical vein. To efficiently direct oxygenated blood to the systemic circulation and minimize oxygen loss, almost 90% of fetal blood flow is diverted past the lungs through anatomic shunts through the foramen ovale and the ductus arteriosus. While the lung rapidly grows its network of small pulmonary arteries during the second half of gestation [1], blood flow in the pulmonary circulation remains highly restricted by hypoxic pulmonary vasoconstriction of small pulmonary arteries, which is reversed at birth by the sudden increase in lung oxygenation when the newborn takes his or her first breath. After birth, the first few breaths induce a rapid decrease in pulmonary vascular resistance and increase in pulmonary vascular flow in response to lung expansion, increased oxygen tension, and increased pH. Pulmonary artery pressure and vascular resistance decrease more slowly, with pulmonary arterial pressure reaching its nadir ~2-3 weeks after birth. However, the responsiveness to hypoxia is retained into adulthood, and pulmonary hypertension can be easily triggered in the newborn period by hypoxic lung disease, apnea, or other causes.© 2012 Elsevier Inc. All rights reserved. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptPediatr Clin North Am. Author manuscript; available in PMC 2013 October 01. DEFINITION AND CLASSIFICATION OF PEDIATRIC PULMONARY HYPERTENSIONPulmonary hypertension is necessary to support gas exchange in the fetus, but if pulmonary arterial pressure is elevated after birth or during infancy or childhood,...

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“…Grisafi et al (10) showed that amniotic fluid stem cells delivered intratracheally can restore partly alveolarization and angiogenesis in an adult rat model of hyperoxia lung injury. Although stem cell therapy is a promising novel therapy for vascular injury-related diseases, studies have demonstrated that only a small portion of transplanted cells can home to the target (11,12).Previous studies suggest that impaired nitric oxide (NO) production may contribute to the pathogenesis of BPD (13,14), and that administration of NO (inhaled NO or NO donor) can improve lung vascular and airspace structure in newborns or BPD models (15)(16)(17). However, the reasons that NO improves lung structures are not well defined, a likely hypothesis is that NO promotes angiogenesis (18).…”

mentioning

confidence: 99%

“…Previous studies suggest that impaired nitric oxide (NO) production may contribute to the pathogenesis of BPD (13,14), and that administration of NO (inhaled NO or NO donor) can improve lung vascular and airspace structure in newborns or BPD models (15)(16)(17). However, the reasons that NO improves lung structures are not well defined, a likely hypothesis is that NO promotes angiogenesis (18).…”

mentioning

confidence: 99%

Combined iNO and endothelial progenitor cells improve lung alveolar and vascular structure in neonatal rats exposed to prolonged hyperoxia

Sun

Qian

2015

Pediatr Res

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Background: Stem cells or inhaled nitric oxide (iNO) are reported to improve lung structures in bronchopulmonary dysplasia (BPD) models. We hypothesized that combined iNO and transplanted endothelial progenitor cells (EPCs) might restore lung structure in rats after neonatal hyperoxia. Methods: Litters were separated into eight groups: room air, hyperoxia, hyperoxia + iNO, hyperoxia + iNO + L-NAME, hyperoxia + EPCs, hyperoxia + EPCs + L-NAME, hyperoxia + EPCs + iNO, and hyperoxia + EPCs + iNO + L-NAME. Litters were exposed to hyperoxia from the 21st day, then, sacrificed. EPCs were injected on the 21st day. L-NAME was injected daily for 7 d from the 21st day. Serum vascular endothelial growth factor (VEGF), radial alveolar count (RAC), VIII factor, EPCs engraftment, lung VEGF, VEGFR2, endothelial nitric oxide (eNOS) and SDF-1 expression, and NO production were examined. results: Hyperoxia exposure led to air space enlargement, loss of lung capillaries, and low expression of VEGF and eNOS. Transplanted EPCs, when combined with iNO, had significantly increased engraftment in lungs, compared to EPCs alone, upon hyperoxia exposure. There was improvement in alveolarization, microvessel density, and upregulation of VEGF and eNOS proteins in the hyperoxia-exposed EPCs with iNO group, compared to hyperoxia alone. conclusion: Combined EPCs and iNO improved lung structures after neonatal hyperoxia. This was associated with the upregulation of VEGF and eNOS expression.B ronchopulmonary dysplasia (BPD) is a chronic lung disease associated with significant mortality and morbidity in premature infants. New BPD is characterized by arrested alveolar and vascular growth (vascular hypothesis of BPD) (1,2). Alveolar formation is a highly coordinated process between the development of airways and pulmonary vasculature (3). Exposure to inflammation caused by excessive O 2 supplementation is hypothesized to interfere with the coordinated process of normal human lung development. Neonatal hyperoxia exposure is known to disrupt alveolar formation and growth, providing a useful model for studying BPD (4).Cell-based therapy is a novel approach that offers much promise in the prevention and treatment of BPD, including embryonic stem cells, mesenchymal stem cells, placental stem cells, umbilical cord stem cells, amniotic fluid and amnionderived cells, and lung progenitor cells. Endothelial progenitor cells (EPCs) are precursors of endothelial cells, which have the capacity of self-renewal and proliferation. EPCs is one of the key cells mediating vascular growth, which can mobilize from bone marrow and home to the site of vascular injuries, promoting neovascularization (5). There is data showing that reduced numbers or dysfunction of EPCs at birth is associated with the development of BPD (6,7). In addition, a reduction in the number of EPCs in the bone marrow, circulation and lungs has also emerged in animal models of BPD (8). Evidences that angiogenic cells treatment can restore lung structure have been demonstrated. Balasubramaniam et al...

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Inhaled Nitric Oxide in Preterm Infants: A Systematic Review

Cited by 117 publications

References 31 publications

Premature Birth and Disease Programming. Contribution of Neonatal Intensive Care

Premature Birth and Disease Programming. Contribution of Neonatal Intensive Care

Pharmacotherapy of Pulmonary Hypertension

Combined iNO and endothelial progenitor cells improve lung alveolar and vascular structure in neonatal rats exposed to prolonged hyperoxia

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