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Mechanisms underlying pulmonary hypertension in a rat model of bronchopulmonary dysplasia.

Robert Peter Jankov

Mechanisms underlying pulmonary hypertension in a rat model of bronchopulmonary dysplasia.

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Published .
Written in English


About the Edition

Abnormalities of the pulmonary circulation have long been recognised to contribute to the morbidity and mortality of bronchopulmonary dysplasia, a common condition of extremely premature infants in which oxidant stress is believed to play a major role and for which there is presently no effective treatment. The hallmark of bronchopulmonary dysplasia is an arrest in alveolar and capillary development. A major circulatory manifestation of bronchopulmonary dysplasia is pulmonary hypertension due to vasoconstriction and increased muscularisation of pulmonary resistance vessels. Animal studies suggest that altered function and structure of the pulmonary circulation may adversely affect alveolar development. Newborn rats exposed to 60% O2 for 14 days develop pulmonary hypertension and parenchymal lung abnormalities that have close morphological similarities to human bronchopulmonary dysplasia. Previous interventional studies in this model have demonstrated that the development of pulmonary hypertension is dependent upon macrophage influx to the lung and up-regulation of endothelin-1, a potent vasoconstrictor peptide. In the studies reported herein, I demonstrated that increased macrophage influx is responsible for the increased reactive oxygen species formation and protein nitration in the lungs of newborn rats exposed to 60% O2 for 14 days. A consequence of oxidant stress is the formation of 8-isoprostane, a bioactive product of lipid peroxidation, which leads to the up-regulation of endothelin-1 production in smooth muscle cells, a major cellular source in the 60% O2-exposed lung. Treatment with a thromboxane A 2 receptor antagonist, but not a cyclooxygenase-2 inhibitor, abrogated these effects, suggesting that the thromboxane A2 receptor ligand causing increased endothelin-1 in the O2-exposed lung was not a cyclooxygenase-2 product, but rather an incidental ligand, such as 8-isoprostane. Finally, the platelet-derived growth factors (-AA and -BB) and insulin-like growth factor-I are identified as mitogens, and endothelin-1 and 8-isoprostane as survival factors, of cultured pulmonary artery smooth muscle cells from infant rats, implicating them as direct mediators of pathological smooth muscle proliferation.

The Physical Object
Pagination171 leaves.
Number of Pages171
ID Numbers
Open LibraryOL20339466M
ISBN 100612918246

The therapeutic promise of multipotent mesenchymal stem/stromal cells (MSC), a population of adult stem cells that can differentiate into cells deriving from mesoderm lineage, is rising [1–3].MSC, historically isolated from bone marrow (BM), emerged in the biomedical field for their proliferative capacity and the potential to generate skeletal-related tissues []. In a recent study, mitochondrial DNA defects caused by hyperoxia dictated the impaired branching morphogenesis and reduced surfactant C expression in fetal rat lung explants (Gebb et al., ).Another study reported that reduced levels of MnSOD expression and activity led to endothelial dysfunction caused by oxidative stress in persistent pulmonary hypertension of the newborn in the .


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Mechanisms underlying pulmonary hypertension in a rat model of bronchopulmonary dysplasia. by Robert Peter Jankov Download PDF EPUB FB2

The underlying mechanism is thought to involve primarily pulmonary artery endothelial cell death followed by the emergence of an apoptosis-resistant cell.

Interestingly, Su-Hx rats returned to normoxia (Su-Hx-Nx) for 10–11 weeks develop neointimal lesions closely resembling human plexogenic by:   Pulmonary hypertension is common in bronchopulmonary dysplasia and is associated with increased mortality and morbidity.

This pulmonary hypertension is due to abnormal microvascular development and pulmonary vascular remodeling resulting in reduced cross‐sectional area of pulmonary by: Pulmonary hypertension (PH) is a common complication of neonatal respiratory diseases including bronchopulmonary dysplasia (BPD), and recent studies have increased awareness that PH worsens the clinical course, morbidity and mortality of by:   Lee HJ, Lee YJ, Choi CW, Lee JA, Kim EK, Kim HS, et al.

Rosiglitazone, a peroxisome proliferator-activated receptor-gamma agonist, restores alveolar and pulmonary vascular development in a rat model of bronchopulmonary dysplasia.

Yonsei Med J. ;55(1): 99– PubMed PubMedCentral CrossRef Google ScholarCited by:   Bronchopulmonary dysplasia (BPD) is a multifactorial disease of preterm infants characterized by alveolar simplification, dysregulated pulmonary vasculature, and pulmonary hypertension.

Invasive mechanical ventilation, hyperoxia, infection, and various other contributing factors acting on the immature lung result in permanent damage to the Author: Sean Leary, Vineet Bhandari.

Pulmonary vascular disease, in particular, pulmonary hypertension (PH), is quite prevalent in children with bronchopulmonary dysplasia (BPD). Recent clinical and preclinical advances in research related to this condition have led to an improved understanding of the pathophysiology of PH and the complex interactions between heart, lung, and pulmonary vasculature in infants with BPD.

This open access book focuses on the molecular mechanism of congenital heart disease and pulmonary hypertension, Morphological Characterization of Pulmonary Microvascular Disease in Bronchopulmonary Dysplasia Caused by Hyperoxia in Newborn Mice.

Hidehiko Nakanishi, Shunichi Morikawa, Shuji Kitahara, Asuka Yoshii, Atsushi Uchiyama, Satoshi. This book describes the molecular mechanisms involved in the development and morphogenesis of the heart, lungs and ductus arteriosus, covering a range of topics such as gene functions, growth factors, transcription factors and cellular interactions, as well as stem cell engineering technologies.

In this Pulmonary Perspective, we review recent data on the importance of the lung circulation, specifically examining the relationship between dysmorphic vascular growth and impaired alveolarization, and speculate on how these new insights may lead to novel therapeutic strategies for bronchopulmonary dysplasia.

Bronchopulmonary dysplasia and emphysema are significant global health problems at the extreme stages of life. and additional studies with appropriate experimental models are required to better define these underlying mechanisms. and structural abnormalities of the vessel wall can contribute to pulmonary hypertension in BPD, leading to.

Bronchopulmonary dysplasia (BPD) is characterized by alveoli simplification and disordered angiogenesis. 1 Despite significant advancements in the.

Bronchopulmonary dysplasia (BPD) is a serious and common chronic lung disease of infancy (), affecting up to one-third of extremely preterm infants and.

Genomics of Bronchopulmonary Dysplasia. The genomics of BPD was first described by Parker et al. 4 who found a high concordance in twin pairs of birth weights less than g. The first definitive study explicitly confirming and quantifying the genetic susceptibility to BPD was conducted by Bhandari et al.

5 In this multicenter retrospective study of twin pairs born at ≤32 weeks of. Keywords: Bronchopulmonary dysplasia; pulmonary hypertension; FGF signaling 1. Introduction There is a rising incidence of preterm births which is one of the leading cause of death in infants younger than 5 years of age [1,2].

Bronchopulmonary dysplasia (BPD) is a common complication for infants born before 30 weeks of gestational age. Rationale: Antenatal factors, such as chorioamnionitis, preeclampsia, and postnatal injury, are associated with an increased risk for bronchopulmonary dysplasia (BPD) and pulmonary hypertension (PH) after preterm birth.

IGF-1 (insulin-like growth factor-1) is markedly decreased in normal preterm infants, but whether IGF-1 treatment can prevent BPD or PH is unknown.

Mechanisms by which poor nutrition impacts lung development are unknown, but alterations in the gut microbiota appear to play a role. In a rodent model, PNGR plus hyperoxia causes BPD and PH and increases intestinal Enterobacteriaceae, Gram-negative organisms that stimulate Toll-like receptor 4.

Abstract. Bronchopulmonary dysplasia (BPD) was first described by Northway et al. in [1]: it is a sequela of variable duration of the respiratory distress syndrome of the newborn and particularly of the premature, whose lungs are deficient in surfactant at birth.

Keywords: Pulmonary hypertension, Bronchopulmonary dysplasia, Vasodilator, Echocardiography, Brain natriuretic peptide Introduction Bronchopulmonary dysplasia (BPD) was first described by Northway et al.

() as a chronic lung disease of preterm infants who required oxygen supply and mechanical ventilation for acute respiratory distress 1). Inhaled nitric oxide improves lung structure and pulmonary hypertension in a model of bleomycin-induced bronchopulmonary dysplasia in neonatal rats Pierre Tourneux,1,2 Neil Markham,1 Gregory Seedorf,1 Vivek Balasubramaniam,1 and Steven H.

Abman1. Pulmonary hypertension in bronchopulmonary dysplasia. Birth Defects Res A Clin Mol Teratol –, Crossref | PubMed Google Scholar; Ambalavanan N, Stanishevsky A, Bulger A, Halloran B, Steele C, Vohra Y, Matalon S.

Titanium oxide nanoparticle instillation induces inflammation and inhibits lung development in mice. Bronchopulmonary Dysplasia (BPD) was first described by Northway and colleagues in as a lung injury in preterm infants resulting from oxygen and mechanical ventilation ().A National Heart, Lung and Blood Institute (NHLBI)-sponsored workshop further defined the disease and suggested research initiatives in ().The pathophysiology of BPD was extensively reviewed by O'Brodovich and.

Bronchopulmonary dysplasia (BPD) remains a major cause of late morbidities and death after preterm birth. BPD is characterized by an arrest of vascular and alveolar growth and high risk for pulmonary hypertension; yet mechanisms contributing to its pathogenesis and early strategies to prevent BPD are poorly understood.

bronchopulmonary dysplasia (BPD) is the chronic lung disease of infancy that often complicates the clinical course and outcomes of preterm newborns ().Infants with severe BPD are at high risk for death, prolonged need for ventilator or oxygen support, pulmonary hypertension, recurrent respiratory infections, abnormal lung function, exercise intolerance, and late neurodevelopmental.

This model provides an opportunity to investigate the mechanisms underlying the development of high pulmonary flow-induced PH or CTEPH.

Acknowledgment This work was supported by the National Natural Science Foundation of China (grant numbers, and ) and in part by the. Introduction. Yearly over 15 million babies are born premature (Bronchopulmonary dysplasia (BPD) is the most common adverse outcome in very preterm neonates with an incidence of 5–68%, depending on the.

Pulmonary hypertension (PH), a condition characterized by elevated pulmonary artery pressure, is usually associated with underlying cardiac or lung disease in children. In particular, PH develops in a subset of infants with bronchopulmonary dysplasia (BPD) [ ].

Pulmonary hypertension is present in a rodent model of bronchopulmonary dysplasia at 21 days but not 6 months of age () Aaron Kleinertz, Robert Conhaim, Taylor Shuster, We hypothesized that RVH would continue into adulthood in a rat model of BPD.

Rats were exposed to 21% or 95% O2 from birth to postnatal day 8. Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension Chapter 11 Morphological Characterization of Pulmonary Microvascular Disease in Bronchopulmonary Dysplasia Caused by Hyperoxia in Newborn Mice Altmetric Badge.

Chapter 12 Involvement of CXCR4 and Stem Cells in a Rat Model of Pulmonary Arterial Hypertension Altmetric. Bronchopulmonary dysplasia has a component of airway pathology, due to hyper-reactivity and airway smooth muscle cell hypertrophy that leads to elevated airway resistance.

11 Since bronchodilators are used to relieve bronchospasm in asthmatic patients and improve dynamic compliance by lowering pulmonary resistance, they have also been used to. Objective. Pulmonary hypertension (PH) worsens the prognosis of bronchopulmonary dysplasia (BPD).

The following items have not been fully established for PH in BPD: clinical characterization, incidence of cardiovascular anomalies (CVAs), response to PH treatment, and outcome. Whether inhaled nitric oxide (iNO) prevents the development of bronchopulmonary dysplasia (BPD) in premature infants is controversial.

In adult rats, bleomycin (Bleo) induces lung fibrosis and pulmonary hypertension, but the effects of Bleo on the developing lung and iNO treatment on Bleo-induced neonatal lung injury are uncertain. Bronchopulmonary dysplasia (BPD) is a developmental lung disorder characterized by simplified alveoli and dysmorphic pulmonary vasculature 1,2,3,4,5.

Bronchopulmonary dysplasia (BPD) is the most common and serious chronic lung disease of preterm infants. The development of pulmonary hypertension (PH) significantly increases the mortality and morbidity of this disease. β-Catenin signaling plays an important role. Retinopathy of prematurity (ROP) and bronchopulmonary dysplasia-associated pulmonary hypertension (BPD-PH) are two conditions that co-exist in many neonates and together contribute to a high rate of morbidity.

Current therapeutic approaches address each condition separately, without considering the potentially shared vascular mechanism. Anthony G. Durmowicz, MD* 2. Kurt R. Stenmark, MD* 1. *Department of Pediatrics, Developmental Lung Biology Laboratory, University of Colorado Health Sciences Center, Denver, CO.

After completing this article, readers should be able to: 1. Explain the physiologic consequences of structural remodeling in chronic pulmonary hypertension. Mesenchymal stromal cells expressing heme oxygenase-1 reverse pulmonary hypertension.

Stem Cells. ; – Crossref Medline Google Scholar; Hansmann G, Fernandez-Gonzalez A, Aslam M, Vitali SH, Martin T, Mitsialis SA, Kourembanas S. Mesenchymal stem cell-mediated reversal of bronchopulmonary dysplasia and associated pulmonary.

This open access book focuses on the molecular mechanism -1 in the pulmonary endothelium 11 Morphological characterization of pulmonary microvascular disease in bronchopulmonary dysplasia caused by hyperoxia in newborn mice 12 Involvement of CXCR4 and stem cells in a rat model of pulmonary arterial hypertension 13 Ca2+ signal through.

This model also further supports the important role of the VEGF system in PH. VEGF receptor inhibition has, besides its aggravating effects on pulmonary hypertension, been shown to induce emphysema when applied in rats as well as a bronchopulmonary dysplasia phenotype when applied in infant rats.

Similar to what was seen in the rat model. Infants with severe BPD have pulmonary hypertension and abnormal vascular development. In model systems of pulmonary hypertension caused by chronic hypoxia in calves, Stenmark has identified vascular adventitial fibroblasts that proliferate and migrate into the media of resistance vessels in the presence of hypoxia (19).

Pulmonary hypertension in infants with bronchopulmonary dysplasia. Korean J Pediatr. ; – doi: /kjp Crossref Medline Google Scholar; Kovacs G, Berghold A, Scheidl S, Olschewski H. Pulmonary arterial pressure during rest and exercise in healthy subjects: a systematic review.

Eur Respir J. Understand better the pathobiology of pulmonary hypertension (PHtn) and the molecular mechanisms of developmental lung injury and repair leading to bronchopulmonary dysplasia (BPD).

Studies in animal physiology and basic molecular biology are validated with studies in infants with lung disease using patient-derived material.bronchopulmonary dysplasia (BPD) is the chronic lung disease of infancy that follows premature birth and is characterized by impaired lung growth due to early lung injury ().BPD is a common and severe complication of preterm birth (19, 59, 66).Infants with BPD have prolonged respiratory insufficiency and are at high risk for pulmonary hypertension (39, 65), lung infections (51, 78), recurrent.An abnormal increase in the amount of oxygen in the tissues and organs.

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