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Academic literature on the topic 'Persistent pulmonary hypertension of the newborn'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Journal articles on the topic "Persistent pulmonary hypertension of the newborn"

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Šebková, S., V. Tomek, P. Zemanová, and Jan Janota. "Heart Failure Treated with Low-dose Milrinone in a Full-term Newborn." Prague Medical Report 113, no. 1 (2012): 58–65. http://dx.doi.org/10.14712/23362936.2015.38.

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A term newborn with a hypocontractile myocardium complicating persistent pulmonary hypertension of the newborn was successfully treated with a low-dose phosphodiesterase III inhibitor milrinone. Echocardiography diagnosed heart failure with a left ventricular ejection fraction of 35% and a left ventricular shortening fraction of 18% and severe persistent pulmonary hypertension of the newborn with oxygenation index of 28. Milrinone was started at an initial dose of 50 mcg/kg, followed by continuous infusion of 0.20 mcg/kg/min. With lowdose milrinone oxygenation index decreased to 3 within 6 hours, left ventricular ejection fraction and left ventricular shortening fraction increased to 57%, and 30%, respectively. Low doses of milrinone might be promising in the treatment of heart failure and persistent pulmonary hypertension of the newborn in term newborns.

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Lister, George. "Persistent Pulmonary Hypertension of the Newborn." International Journal of Technology Assessment in Health Care 7, S1 (January 1991): 66–69. http://dx.doi.org/10.1017/s0266462300012538.

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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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Hussain, Manzoor. "Persistent Pulmonary Hypertension of Newborn (PPHN)." Dhaka Shishu (Children) Hospital Journal 35, no. 2 (October 12, 2020): 90–93. http://dx.doi.org/10.3329/dshj.v35i2.49687.

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Mathew, Bobby, and Satyan Lakshminrusimha. "Persistent Pulmonary Hypertension in the Newborn." Children 4, no. 8 (July 28, 2017): 63. http://dx.doi.org/10.3390/children4080063.

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Thérèse, Perreault. "Persistent pulmonary hypertension of the newborn." Paediatric Respiratory Reviews 7 (January 2006): S175—S176. http://dx.doi.org/10.1016/j.prrv.2006.04.211.

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Walsh, Michele C., and Eileen K. Stork. "PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN." Clinics in Perinatology 28, no. 3 (September 2001): 609–27. http://dx.doi.org/10.1016/s0095-5108(05)70109-3.

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Walsh-Sukys, Michele C. "Persistent Pulmonary Hypertension of the Newborn." Clinics in Perinatology 20, no. 1 (March 1993): 127–43. http://dx.doi.org/10.1016/s0095-5108(18)30415-9.

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Hammerman, Cathy, David Yousefzadeh, Jung-Hwan Choi, and Kim-chi Bui. "Persistent Pulmonary Hypertension of the Newborn." Clinics in Perinatology 16, no. 1 (March 1989): 137–56. http://dx.doi.org/10.1016/s0095-5108(18)30660-2.

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Ostrea, Enrique M., Esterlita T. Villanueva-Uy, Girija Natarajan, and Herbert G. Uy. "Persistent Pulmonary Hypertension of the Newborn." Pediatric Drugs 8, no. 3 (2006): 179–88. http://dx.doi.org/10.2165/00148581-200608030-00004.

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Lakshminrusimha, S., and M. Keszler. "Persistent Pulmonary Hypertension of the Newborn." NeoReviews 16, no. 12 (December 1, 2015): e680-e692. http://dx.doi.org/10.1542/neo.16-12-e680.

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Dissertations / Theses on the topic "Persistent pulmonary hypertension of the newborn"

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Chaudhry, Adil Anthony. "Transient postnatal pulmonary arterial smooth muscle cytoskeletal disassembly and its functional implications." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327049.

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Villamor, Zambrano Eduardo. "Persistent pulmonary hypertension of the newborn a point of view from vascular pharmacology /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 2001. http://arno.unimaas.nl/show.cgi?fid=6985.

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Cruz, Belen A. "Oxygen Tension Modulates Growth Of Ovine Newborn Pulmonary Vascular Smooth Muscle Cells." Scholarship @ Claremont, 2014. http://scholarship.claremont.edu/scripps_theses/333.

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Background: Platelet activating factor (PAF) is a phospholipid synthesized by the action of phospholipase A2 and acetyl transferase. PAF possesses a wide range of biological activities. In the lung of the fetus and newborn, PAF binds to its G protein couple receptor to evoke its biological activities via a well-defined signaling pathway. High levels of PAF receptor (PAFr) activity in fetal ovine lung vascular smooth muscle cells (PVSMC) at baseline has previously been demonstrated, a finding that is further perpetuated by conditions of hypoxia similar to fetal lung environment. Additionally in fetal ovine PVSMC, a cross-talk between PAFr-mediated cell signaling and activity of the vasodilator cyclic nucleotides cGMP and cAMP acting via their respective receptors protein kinase (PK) G and PKA has been shown. The interaction of PAF with its receptor has been implicated in the pathogenesis of persistent pulmonary hypertension in the newborn (PPHN) which has a high incidence of hospitalization and death of newborn infants. Successful transition of fetus to newborn life entails a mechanism whereby vasoconstrictors necessary for fetal existence are abrogated in the immediate newborn. Hypothesis: We hypothesize that PPHN results from the failure to down regulate PAFr- mediated activity and /or failure to up-regulate activity of the vasodilators cGMP and cAMP. PPHN is triggered by chronic intrauterine or postnatal hypoxia. Then newborn PVSMC undergo hyperplasia and hypertrophy, which over time, results in irreversible vascular remodeling. Methods: My study aims to employ in vitro models to delineate the consequences of PAF-PAFr mediated pathway in the pharmacological effects of the cAMP-PKA and cGMP-PKG signaling and the involvement of this cross-talk in the pathogenesis of PPHN. I modeled my cell culture studies to mimic the low oxygen environment of fetal lungs (hypoxia), the normal oxygen environment of newborn lungs (normoxia) and high oxygen environment (hyperoxia) to which the newborn lung may be exposed in incidental clinical condition of PPHN. I studied the effect of PAF, a vasoconstrictor, cAMP/cGMP, vasodilators, and other inhibitors of the PAFr pathway on growth of newborn PVSMC, by DNA synthesis, and measured their effects on expression of mitogenic and non-mitogenic proteins. Results: We found that both hypoxia and hyperoxia decreased cell growth even in the presence of PAF which up-regulates cell growth in fetal PVSMC. Also PAF treatment of cells resulted in down regulation of the vasodilator proteins, PKA and PKG. Conclusion: Our data suggests that in the lung of the newborn a high activity of PAF-PAFr mediated activities will worsen the condition of PPHN imposed on the newborn lung by environmental or therapeutic conditions. We can speculate that, in the long run, these findings may translate into the establishment of less toxic protein-based management of PPHN.

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McAlpine, Alastair. "The use of inhaled nitric oxide to treat persistent pulmonary hypertension of the newborn in a tertiary public hospital in South Africa from 2010-2014: morbidity, mortality and cost." Master's thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29788.

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Background and rationale: Inhaled nitric oxide (iNO) is recommended for the treatment of severe persistent pulmonary hypertension of the newborn (PPHN) because it reduces the need for extracorporeal membrane oxygenation (ECMO). There is insufficient evidence that iNO reduces mortality in the absence of ECMO. Although neonates in some South African public hospitals have access to iNO, ECMO is not available. Oral sildenafil can be effective in settings where iNO is not available, but its effect on outcome and cost of treatment in this setting have not been described. The literature review in the first part of this thesis describes five studies reporting short-term outcomes of PPHN in the absence of ECMO. No studies from South Africa were identified. Only two studies described outcomes after iNO – the coadministration of Sildenafil with iNO was only reported in one small study. There were insufficient published data to guide management in settings where ECMO is not available. Aim: To describe a cohort of term and near term neonates with PPHN who were treated with iNO, with or without sildenafil, in a tertiary neonatal unit in South Africa Objectives: (i) to describe the characteristics at birth, the clinical course, and shortterm outcomes; (ii) to determine if any variables were associated with mortality; (iii) to describe the relationship between the use of sildenafil and cost of care, represented by the duration of intubation and iNO use; and (iv) to describe the frequency of sildenafil prescription. Methods. A retrospective review was carried out on folders of neonates with PPHN who were treated with iNO in Groote Schuur Hospital, Cape Town, South Africa, between January 2010 and December 2014. Results. Forty neonates were included – most were full term (85%). Meconium aspiration syndrome (MAS) was the commonest cause of PPHN (50%), followed by intrapartum hypoxia (20%), sepsis (17.5%), pulmonary hypoplasia (7.5%) and idiopathic (5%). Fourteen neonates (35%) died. Pulmonary hypoplasia and pneumothorax were associated with mortality (p=0.037 and p=0.004 respectively). An FiO2 of 1.0 and an iNO dose of ≥ 20 ppm at 24 and 48 hours respectively, both predicted death (specificity 89% vs. 100%, sensitivity 67% vs. 43% and p=0.003 vs. p=0.007 respectively). Sildenafil was prescribed more often after 2011 (83% vs. 65%) and was associated with increased survival (p=0.018) – early administration was associated with a shorter time to extubation (p=0.012) and a shorter course of iNO (p=0.044). Conclusion. The treatment of PPHN with iNO in the absence of ECMO was associated with high mortality, particularly in neonates with congenital lung abnormalities. The FiO2 and iNO requirements at 24 and 48 hours respectively could be used to identify neonates who are unlikely to benefit from continued treatment. Sildenafil was prescribed with increasing frequency during the study. The combination of iNO with sildenafil was associated with more cost-effective care and improved short term outcomes. These findings provide a potential basis for costsaving measures and resource allocation.

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Sharma, Dyuti. "Nouvelles approches thérapeutiques de la pathologie pulmonaire par les suppléments alimentaires en période périnatale." Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S066/document.

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La dysplasie broncho-pulmonaire (DBP), complication fréquente de la prématurité, atteint 30% des nouveau-nés de faible poids de naissance. L’hypertension artérielle pulmonaire persistante du nouveau-né (HTAPP), associé ou non à la DBP, résulte d’une mauvaise adaptation à la vie extra-utérine et survient dans diverses situations pathologiques (prématurité, sepsis, inhalation de méconium, hernie diaphragmatique congénitale…). Ces 2 pathologies sont grevées d’une morbidité et d’une mortalité importante en période périnatale. En effet, certaines situations d’HTAPP ou de DBP sévères restent réfractaires aux thérapeutiques actuelles.Les acides gras polyinsaturés oméga 3 (AGPI ω-3) sont des nutriments aux propriétés bénéfiques sur le système circulatoire et pulmonaire, mais également sur le développement fœtal, démontrés par de nombreuses études expérimentales et cliniques. La déhydroépiandrostérone (DHEA) est une hormone stéroïdienne dont le taux de sécrétion chez l’homme diminue avec l’âge. Des études récentes ont démontré un effet cardio-protecteur mais également un effet vasodilatateur pulmonaire et préventif de lésions de DBP dans des modèles expérimentaux.Les buts de notre travail étaient 1) d’étudier l’effet d’une supplémentation en AGPI ω-3 dans un modèle expérimental de DBP induite par hyperoxie chez le raton, 2) d’étudier l’effet circulatoire d’injection d’AGPI ω-3 (in vivo) dans un modèle d’étude de la circulation pulmonaire chez le fœtus de brebis chroniquement instrumenté, et d’étudier les mécanismes d’action AGPI ω-3 (anneaux vasculaires isolés) , enfin 3) d’étudier l’effet circulatoire de la DHEA (in vivo) dans le modèle de fœtus de brebis et d’étudier les mécanismes d’actions de la DHEA sur la circulation pulmonaire fœtale (in vivo)._x000D_Nous avons démontré que la supplémentation par voie orale en AGPI ω-3 de rates gestantes à la fin de la gestation et après la naissance permettait de prévenir, chez les ratons nouveau-nés, les lésions de DBP induites par une exposition chronique à l’hyperoxie. Ces lésions étaient retrouvées dans les groupes contrôles (eau et AGPI ω-6). Cette étude n’avait pas retrouvée d’effet bénéfique des AGPI ω-3 sur le remodelage vasculaire induit.L’injection d’acide eicosapentaènoique (EPA) chez le fœtus de brebis a révélé un effet vasodilatateur pulmonaire puissant avec une baisse significative et prolongée des résistances vasculaires pulmonaires (RVP), en comparaison à l’injection d’acide docosahéxaènoique (DHA) ou de l’excipient (faible dose d’éthanol). L’effet vasorelaxant de l’EPA sur des anneaux isolés pré-contractés était plus important que celui du DHA à dose équivalente, et il était dose- et endothélium-dépendent. Enfin, cet effet impliquait la voie de production du NO puisqu’il était diminué lors du traitement des anneaux par le L-Nitro-Arginine (LNA), inhibant la NO synthase.L’étude de perfusion en bolus de DHEA dans le lit pulmonaire vasculaire chez le fœtus de brebis instrumenté mettait en évidence un effet vasodilatateur bref. Cet effet était dose-dépendant avec une baisse plus prononcée des RVP et une durée plus importante pour des doses de DHEA plus importantes. Enfin l’étude des mécanismes d’action retrouvait une inhibition de l’effet de la DHEA par le LNA, démontrant une action vasodilatatrice par activation de production du NO.L’ensemble de ces travaux permet de suggérer que les AGPI ω-3 représentent des nutriments intéressants en période périnatale (grossesse, allaitement et per os), notamment en traitement préventif dans les situations à risque de DBP, ou curatif en cas d’HTAPP. La DHEA reste une piste dans le traitement de l’HTAP, mais semble pour l’instant plus difficile à instaurer en clinique humaine
Bronchopulmonary dysplasia (BPD), a common complication of prematurity, reached in 30% of newborns with very low birth weight. Persistent pulmonary hypertension of the newborn (PPHN), with or without BPD, results in poor adaptation to extrauterine life and occurs in various pathological conditions such as prematurity, sepsis, inhaled meconium, or diaphragmatic hernia Congenital. The mortality and morbidities of these two diseases are high in the perinatal period. Severe PPHN or BPD are refractory to current treatment.Polyunsaturated fatty acids omega-3 (ω-3 PUFA) are nutrients with beneficial properties on the circulatory and pulmonary system, but also on fetal development, demonstrated by many experimental and clinical studies. Dehydroepiandrosterone (DHEA) is a steroid hormone whose secretion levels in humans decreases with age. Recent studies have demonstrated a cardio-protective effect of diet DHEA supplementation but also a pulmonary vasodilator and preventive effect of DBP injury in experimental models.The aims of our study were : 1) to study the effect of PUFA ω-3 supplementation in an experimental model of hyperoxia-induced DBP in pups; 2) to study effect on pulmonary circulation of infusion of ω-3 PUFAs (in vivo) in model of chronically instrumented fetal sheep, and to analyze the mechanisms of action of ω-3 PUFA (isolated vascular rings); and finally 3) to study the in vivo effect of DHEA in fetal pulmonary circulation in the same model of fetal sheep and to understand the mechanisms of action of DHEA._x000D_We have demonstrated that supplementation with diet PUFA ω-3 on pregnant rats at the end of gestation and after birth prevent BPD injuries induced by chronic exposure to hyperoxia in pups. These lesions were found in the control groups (water and ω-6 PUFA). ω-3 PUFA supplementation did not prevent vascular remodeling.Infusion of eicosapentaenoic acid (EPA) in sheep fetus showed a potent pulmonary vasodilator effect as compared to docosahexaenoic acid (DHA) or excipient (low dose of ethanol). Vasorelaxant effect of EPA on pre-contracted isolated rings was more important than DHA at equivalent dose, and was dose- and endothelium-dependent. This effect involves NO production.Bolus DHEA perfusion in the pulmonary vascular bed study on instrumented fetal sheep highlighted an acute vasodilator effect. This effect was dose-dependent with a more pronounced and sustained decrease in PVR at highest doses of DHEA. Finally, mechanisms of action study found an inhibition of the effect of DHEA by the LNA, indicating that DHEA-induced vasodilation is NO dependant.Taken together, our results suggest that supplementation with ω-3 PUFAs and DHEA within the perinatal period may prevent BPD and PPHN in high risk conditions including preterm birth, premature rupture of the membrane or intrauterine growth restriction

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Vuckovic, Aline. "Prenatal modulation of the developing lung in congenital diaphragmatic hernia: functional, morphological, and biological consequences for the neonatal lung." Doctoral thesis, Universite Libre de Bruxelles, 2016. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/228906.

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INTRODUCTION. Congenital diaphragmatic hernia (CDH) combines a congenital malformation of the diaphragm with lung hypoplasia, leading to severe respiratory distress and intractable pulmonary hypertension of the newborn. Despite advances in prenatal diagnosis and neonatal intensive care, CDH is associated with high mortality and devastating morbidities. In the absence of curative treatment, numerous prenatal therapies have been used experimentally with varying success. So far, only fetal tracheal occlusion has been tested in clinical trials, but the consequences for the human lung are poorly known. AIMS. To further characterize the rabbit model of CDH, which was subsequently used to assess the effects of prenatal therapies on airway and pulmonary vascular development, including tracheal occlusion, and two novel approaches, perfluorooctylbromide and an activator of soluble guanylate cyclase (BAY 41–2272), which were given through tracheal instillation.METHODS. After a diaphragmatic incision during the pseudoglandular stage, fetal rabbits were randomized against placebo/sham operation during the saccular stage for tracheal occlusion, perfluorocarbon or BAY 41–2272. At term operated fetuses and controls were subject to evaluation of lung mechanics and/or hemodynamics as well as postmortem lung analyses. Human fetal and neonatal lung tissue, including controls and CDH with tracheal occlusion or expectant management, was analyzed histologically and biochemically.RESULTS. The rabbit model of CDH was characterized by reduced lung volumes and impaired compliance, disorders of elastin deposition within alveolar walls, and downregulation of elastogenesis-related genes. Moreover, this model reproduced features of pulmonary hypertension, including high right ventricular pressure and level of N-terminal-pro-B type natriuretic peptide, remodeling of pulmonary arterioles, decreased alveolar capillary density, and downregulation of vasodilation-related genes. In the rabbit model, lung distension caused by tracheal occlusion improved alveolar formation and elastogenesis, yet without correction of lung mechanical parameters. Tracheal occlusion increased also the expression of other extracellular matrix components, which reflected myofibroblast activity, and reduced the transcription of surfactant-associated proteins. Human neonatal lungs exposed to fetal tracheal occlusion displayed alveolar deposits of collagen and myofibroblasts. In human CDH as well as in the rabbit model of CDH, tracheal occlusion enhanced the pulmonary expression of transforming growth factor-β (TGFβ) and Rho kinase−associated proteins to the detriment of activation of SMAD2/3, which is normally detected in human lungs with advancing gestation. As an alternative to tracheal occlusion, pulmonary distension by perfluorocarbon in the fetal rabbit model of CDH improved lung mechanics and alveolar elastogenesis without transcriptional changes in extracellular matrix, surfactant protein genes or TGFβ. Finally, intratracheal instillation of BAY 41–2272 in the rabbit fetuses with CDH improved hemodynamics, reduced medial hypertrophy of pulmonary arterioles, and increased capillary bed formation by stimulating endothelial cell proliferation.CONCLUSIONS. In the fetal rabbit model of CDH, poor lung function after tracheal occlusion is compatible with activation of TGFβ and imbalance in extracellular matrix and epithelial homeostasis. In human CDH newborns treated by fetal tracheal occlusion, changes in the pulmonary interstitium and impaired TGFβ signaling raise the question of disturbances of postnatal lung development induced by tracheal occlusion. As potential alternatives to tracheal occlusion, prenatal perfluorocarbon improves lung hypoplasia, whereas prenatal BAY 41–2272 attenuates pulmonary hypertension.
Doctorat en Sciences médicales (Médecine)
info:eu-repo/semantics/nonPublished

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Aubry, Estelle. "Nouvelles stratégies de prise en charge de l'hypertension pulmonaire périnatale." Phd thesis, Université du Droit et de la Santé - Lille II, 2012. http://tel.archives-ouvertes.fr/tel-00762661.

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L'hypertension artérielle pulmonaire (HTAP) correspond à une augmentation des résistances artérielles pulmonaires, avec dans les formes les plus graves, une défaillance cardiaque droite. L'HTAP persistante du nouveau-né (HTAPP) est estimée à 2/100 naissances en France. L'adaptation cardio-respiratoire à la naissance implique le déclenchement simultané de plusieurs phénomènes non complètements compris. Notre travail avait pour but d'approfondir les connaissances sur la régulation pulmonaire périnatale et d'envisager de nouvelles possibilités thérapeutiques. Ainsi, nous avons mis en évidence in vivo une vasoconstriction pulmonaires chez le fœtus lors du tabagisme passif maternel, par blocage de la voie du NO. De même, nous avons pu montrer l'effet vasoconstricteur de l'apeline sur les artères pulmonaires de fœtus de brebis. Cet effet semble dose dépendant, inhibé par l'action des inhibiteurs calciques. Au contraire nous avons mis en évidence un effet vasodilatateur de la Déhydroépiandrostérone (DHEA). Cette action est médiée par la voie du NO. Parallèlement, nous avons montré que les acides gras poly insaturés ω 3 (AGPIω3) entrainaient une vasodilatation pulmonaire, se prolongeant au delà d'une heure après l'arrêt de la perfusion. Cet effet est médié par l'ouverture des canaux potassiques et indépendant de la voie du NO. Parmi les AGPIω3, nous avons établi que l'acide eicosapentaénoïque (EPA) qui induit cette réponse sans effet délétère sur la circulation systémique, ni l'oxygénation tissulaire. Enfin, nous avons établi que l'occlusion trachéale (OT) anténatale, traitement proposé pour certaine hypoplasie pulmonaire malformative, n'altère pas le débit pulmonaire, en favorisant la dilatation pulmonaire. Mais en cas d'OT prolongée, ces effets sont en partie masqués par les effets mécaniques de la pression intraluminale. Ainsi grâce à ces travaux, nous avons avancé dans la compréhension de l'adaptation de la circulation pulmonaire de la vie intra à la vie extra utérine. Ils permettent aussi de proposer de nouvelles thérapeutiques comme la supplémentation en AGPIω 3 des femmes attendant un enfant à risque d'HTAP, et d'envisager de nouvelles voies de recherche thérapeutique comme la voie de l'apeline.

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Makanga, Martine. "Pathobiologie de la hernie diaphragmatique congénitale expérimentale induite par l'exposition au nitrofène chez le rat." Doctoral thesis, Universite Libre de Bruxelles, 2015. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209093.

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Martinho, Ana Sofia Saraiva. "Persistent Pulmonary Hypertension of the Newborn: Pathophysiological mechanisms and novel therapeutic approaches." Dissertação, 2020. https://hdl.handle.net/10216/128845.

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A hipertensão pulmonar persistente do recém-nascido (HPPRN) é uma das principais causas de morbilidade e mortalidade neonatal. É caracterizada pela elevação sustentada da resistência vascular pulmonar (RVP), que impede o aumento do fluxo sanguíneo pulmonar. Assim, estes recém-nascidos não estabelecem uma adequada oxigenação sanguínea, o que pode resultar em dificuldade respiratória grave, hipoxemia e eventualmente morte. O óxido nítrico inalado (NOi), o único vasodilatador pulmonar aprovado para o tratamento da HPPRN, constitui, com a terapêutica de suporte, a base do seu tratamento. No entanto, cerca de 40% destes recém-nascidos são resistentes à sua ação. A patogénese da HPPRN é multifatorial. Os dois mecanismos de base que explicam o aumento da RVP são a vasoconstrição pulmonar e a remodelagem vascular. Uma melhor compreensão da fisiopatologia da HPPRN é essencial para que possam surgir novas terapêuticas dirigidas e mais eficazes. O sildenafil, as prostaglandinas, a milrinona e o bosentan, atuando como vasodilatadores, bem como os glicocorticóides, que desempenham um papel na redução da inflamação, demonstraram potenciais efeitos benéficos em recém-nascidos com HPPRN. Adicionalmente, evidência experimental em modelos animais de HPPRN sustenta o uso futuro de terapêuticas emergentes, tais como ativadores/estimuladores da GCs, L-citrulina, inibidores da Rho-cínase, agonistas do PPAR-γ, SODrh, análogos de BH4, LC-PUFAs ω-3, antagonistas do recetor 5-HT2A e VEGFrh. Esta revisão foca-se no conhecimento atual e recente das vias de sinalização alternativas envolvidas na patogénese da HPPRN. Adicionalmente, revemos os fatores de risco pré-natais, perinatais e neonatais que preveem um maior risco HPPRN e que, por sua vez, poderão ajudar a melhor entender a sua fisiopatologia. Por fim, focámo-nos nos últimos progressos referentes à evidência clínica e experimental quanto ao uso de potenciais abordagens terapêuticas para o tratamento da HPPRN.
Persistent pulmonary hypertension of the newborn (PPHN) is one of the main causes of neonatal morbidity and mortality. It is characterized by sustained elevation of pulmonary vascular resistance (PVR), preventing an increase in pulmonary blood flow. The affected neonates fail to establish blood oxygenation, precipitating severe respiratory distress, hypoxemia and eventually death. Inhaled nitric oxide (iNO), the only approved pulmonary vasodilator for PPHN, constitutes, alongside supportive therapy, the basis of its treatment. However, nearly 40% of infants are iNO-resistant. The pathogenesis of PPHN is multifactorial. The cornerstones of increased PVR are pulmonary vasoconstriction and vascular remodeling. A better understanding of PPHN pathophysiology may enlighten targeted and more effective therapies. Sildenafil, prostaglandins, milrinone and bosentan, acting as vasodilators, besides glucocorticoids, playing a role on reducing inflammation, have all shown potential beneficial effects on PPHN newborns. Furthermore, experimental evidence in PPHN animal models supports prospective use of emergent therapies, such as sGC activators/stimulators, L-citrulline, Rho-kinase inhibitors, PPAR-γ agonists, rhSOD, BH4 analogues, ω-3 LC-PUFAs, 5-HT2A receptor antagonists and rhVEGF. This review focuses on current knowledge on alternative and novel pathways involved in PPHN pathogenesis. We also enlighten prenatal, perinatal and neonatal risk factors that predict higher risk for PPHN, which may allow better understanding of its underlying pathophysiology. Moreover, we focus on recent progress regarding experimental and clinical evidence on potential therapeutic approaches for PPHN.

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Martinho, Ana Sofia Saraiva. "Persistent Pulmonary Hypertension of the Newborn: Pathophysiological mechanisms and novel therapeutic approaches." Master's thesis, 2020. https://hdl.handle.net/10216/128845.

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A hipertensão pulmonar persistente do recém-nascido (HPPRN) é uma das principais causas de morbilidade e mortalidade neonatal. É caracterizada pela elevação sustentada da resistência vascular pulmonar (RVP), que impede o aumento do fluxo sanguíneo pulmonar. Assim, estes recém-nascidos não estabelecem uma adequada oxigenação sanguínea, o que pode resultar em dificuldade respiratória grave, hipoxemia e eventualmente morte. O óxido nítrico inalado (NOi), o único vasodilatador pulmonar aprovado para o tratamento da HPPRN, constitui, com a terapêutica de suporte, a base do seu tratamento. No entanto, cerca de 40% destes recém-nascidos são resistentes à sua ação. A patogénese da HPPRN é multifatorial. Os dois mecanismos de base que explicam o aumento da RVP são a vasoconstrição pulmonar e a remodelagem vascular. Uma melhor compreensão da fisiopatologia da HPPRN é essencial para que possam surgir novas terapêuticas dirigidas e mais eficazes. O sildenafil, as prostaglandinas, a milrinona e o bosentan, atuando como vasodilatadores, bem como os glicocorticóides, que desempenham um papel na redução da inflamação, demonstraram potenciais efeitos benéficos em recém-nascidos com HPPRN. Adicionalmente, evidência experimental em modelos animais de HPPRN sustenta o uso futuro de terapêuticas emergentes, tais como ativadores/estimuladores da GCs, L-citrulina, inibidores da Rho-cínase, agonistas do PPAR-γ, SODrh, análogos de BH4, LC-PUFAs ω-3, antagonistas do recetor 5-HT2A e VEGFrh. Esta revisão foca-se no conhecimento atual e recente das vias de sinalização alternativas envolvidas na patogénese da HPPRN. Adicionalmente, revemos os fatores de risco pré-natais, perinatais e neonatais que preveem um maior risco HPPRN e que, por sua vez, poderão ajudar a melhor entender a sua fisiopatologia. Por fim, focámo-nos nos últimos progressos referentes à evidência clínica e experimental quanto ao uso de potenciais abordagens terapêuticas para o tratamento da HPPRN.
Persistent pulmonary hypertension of the newborn (PPHN) is one of the main causes of neonatal morbidity and mortality. It is characterized by sustained elevation of pulmonary vascular resistance (PVR), preventing an increase in pulmonary blood flow. The affected neonates fail to establish blood oxygenation, precipitating severe respiratory distress, hypoxemia and eventually death. Inhaled nitric oxide (iNO), the only approved pulmonary vasodilator for PPHN, constitutes, alongside supportive therapy, the basis of its treatment. However, nearly 40% of infants are iNO-resistant. The pathogenesis of PPHN is multifactorial. The cornerstones of increased PVR are pulmonary vasoconstriction and vascular remodeling. A better understanding of PPHN pathophysiology may enlighten targeted and more effective therapies. Sildenafil, prostaglandins, milrinone and bosentan, acting as vasodilators, besides glucocorticoids, playing a role on reducing inflammation, have all shown potential beneficial effects on PPHN newborns. Furthermore, experimental evidence in PPHN animal models supports prospective use of emergent therapies, such as sGC activators/stimulators, L-citrulline, Rho-kinase inhibitors, PPAR-γ agonists, rhSOD, BH4 analogues, ω-3 LC-PUFAs, 5-HT2A receptor antagonists and rhVEGF. This review focuses on current knowledge on alternative and novel pathways involved in PPHN pathogenesis. We also enlighten prenatal, perinatal and neonatal risk factors that predict higher risk for PPHN, which may allow better understanding of its underlying pathophysiology. Moreover, we focus on recent progress regarding experimental and clinical evidence on potential therapeutic approaches for PPHN.

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Books on the topic "Persistent pulmonary hypertension of the newborn"

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Lazar, Alina. Congenital Pulmonary Airway Malformation. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0015.

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Respiratory distress in infants may be caused by perinatal events and physiologic changes (e.g., lung immaturity, meconium aspiration, and persistent pulmonary hypertension); infectious processes; cardiovascular, neurologic, and metabolic abnormalities; as well as congenital lung abnormalities. Some of these may coexist, further complicating the diagnosis, clinical course, and management of the affected infant. Sound anesthetic management of congenital lung abnormalities requires a clear understanding of the pathophysiology of lung lesions and, in particular, the consequences of positive-pressure ventilation in patients with cystic and emphysematous lesions. Also critical is an appreciation for the physiologic differences in children undergoing thoracic surgery, indications for one-lung ventilation, age-appropriate lung isolation techniques, potential respiratory and cardiovascular complications that may occur during pediatric thoracic surgery, and the optimal choices for postoperative analgesia.

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Book chapters on the topic "Persistent pulmonary hypertension of the newborn"

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Steinhorn, Robin H. "Persistent Pulmonary Hypertension of the Newborn." In PanVascular Medicine, 1–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-37393-0_157-1.

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Gien, Jason, John P. Kinsella, and Steven H. Abman. "Persistent Pulmonary Hypertension of the Newborn." In Neonatology, 933–62. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-29489-6_208.

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Schumacher, Robert E., and Steven M. Donn. "Persistent Pulmonary Hypertension of the Newborn." In Manual of Neonatal Respiratory Care, 565–76. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2155-9_64.

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O’Connell, Joseph, Robert E. Schumacher, and Steven M. Donn. "Persistent Pulmonary Hypertension of the Newborn." In Manual of Neonatal Respiratory Care, 599–604. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39839-6_72.

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Stopfkuchen, H. "Persistent Pulmonary Hypertension in the Newborn." In Update in Intensive Care and Emergency Medicine, 467–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-82801-0_76.

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Mercier, J. C., A. T. Dinh-Xuan, and S. H. Abman. "Persistent Pulmonary Hypertension of the Newborn." In Role of Nitric Oxide in Sepsis and ADRS, 355–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79920-4_23.

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Jain, Amish, and Mark K. Friedberg. "Persistent Pulmonary Hypertension of the Newborn." In Visual Guide to Neonatal Cardiology, 350–58. Chichester, UK: John Wiley & Sons Ltd, 2018. http://dx.doi.org/10.1002/9781118635520.ch57.

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Stopfkuchen, H. "Persistent Pulmonary Hypertension of the Newborn." In Update in Intensive Care and Emergency Medicine, 192–202. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83010-5_18.

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Gien, Jason, John P. Kinsella, and Steven H. Abman. "Persistent Pulmonary Hypertension of the Newborn." In Neonatology, 1–30. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-18159-2_208-1.

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Stenmark, K. R., M. G. Frid, and E. C. Dempsey. "Persistent Pulmonary Hypertension of the Newborn." In Update in Intensive Care and Emergency Medicine, 11–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80227-0_2.

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Conference papers on the topic "Persistent pulmonary hypertension of the newborn"

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Dadlani, Gul, Vanessa M. Perez, Jennifer Leshko, Ivan Wilmot, Jim Galas, Kathryn Nardell, Thieu Nguyen, and Rajan Wadhawan. "Intravenous Treprostinil Therapy For The Acute Management Of Persistent Pulmonary Hypertension Of The Newborn." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3396.

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Joshi, Swosti, Vilmaris Quinones Cardona, and Ogechukwu Menkiti. "Utility of Vasopressin Rescue Therapy in Neonates with Persistent Pulmonary Hypertension of the Newborn." In AAP National Conference & Exhibition Meeting Abstracts. American Academy of Pediatrics, 2021. http://dx.doi.org/10.1542/peds.147.3_meetingabstract.749.

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Kaluarachchi, Dinushan, Jessica C. Smith, Bruce Bedell, Jonathan Klein, John Dagle, Kelli Ryckman, and Jeffrey Murray. "Polymorphisms in the Urea Cycle Enzyme Genes Are Associated with Persistent Pulmonary Hypertension of Newborn." In Selection of Abstracts From NCE 2015. American Academy of Pediatrics, 2017. http://dx.doi.org/10.1542/peds.140.1_meetingabstract.73.

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Lakshminrusimha, Satyan, Bobby Mathew, Karen A. Wynn, Jayasree Nair, Rita M. Ryan, James A. Russell, and Daniel D. Swartz. "Inhaled Nitric Oxide (iNO) Prevents Hypoxic Pulmonary Vasoconstriction In Lambs With Persistent Pulmonary Hypertension Of The Newborn (PPHN)." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3894.

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Konduri, G. G., U. Rana, B. Entringer, E. Callan, R. J. Teng, and T. Michalkiewicz. "Pulmonary Artery Endothelial Cell Phenotype Switch Impairs Angiogenesis in the Lungs in Persistent Pulmonary Hypertension of the Newborn." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5868.

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Li, Yumei, Chaoying Yan, Chunfeng Yang, and Chunlai Dai. "Clinical study on high risk factors of 57 cases of persistent pulmonary hypertension of the newborn." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027977.

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Wedgwood, Stephen, Satyan Lakshminrusimha, James Russell, Paul T. Schumacker, and Robin Steinhorn. "Increased H2O2 Generation Is Associated With Increased NOX4/P22PHOX Expression In Persistent Pulmonary Hypertension Of The Newborn (PPHN)." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5491.

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Ryan, RM, J. Pabalan, SP Nayak, and S. Lakshminrusimha. "Can Methemoglobin Levels Be Used To Predict Response to Inhaled Nitric Oxide in Persistent Pulmonary Hypertension of the Newborn (PPHN)?." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5968.

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Sharma, Megha, Adeleye J. Afolayan, Ru-Jeng Teng, and Girija G. Konduri. "Downregulation of Cgmp Mediated Mitochondrial Biogenesis Contributes to Impaired Angiogenesis in Fetal Lambs with Persistent Pulmonary Hypertension of the Newborn (pphn)." In Selection of Abstracts From NCE 2016. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/peds.141.1_meetingabstract.513.

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Hengst, Meike, Nicolaus Schwerk, Jost Wigand Richter, Hans Fuchs, Lars Welzing, Mathias Klemme, and Matthias Griese. "Diffuse pulmonary development disorders- Molecular definable causes of pulmonary hypertension in the mature newborn." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1867.

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Reports on the topic "Persistent pulmonary hypertension of the newborn"

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Xin, Liu, He Haiying, Wu Haihuan, and Xin Yuemei. Meta analysis of milrinone in the treatment of persistent pulmonary hypertension in newborns. International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0014.

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Viswanathan, Meera, Jennifer Cook Middleton, Alison Stuebe, Nancy Berkman, Alison N. Goulding, Skyler McLaurin-Jiang, Andrea B. Dotson, et al. Maternal, Fetal, and Child Outcomes of Mental Health Treatments in Women: A Systematic Review of Perinatal Pharmacologic Interventions. Agency for Healthcare Research and Quality (AHRQ), April 2021. http://dx.doi.org/10.23970/ahrqepccer236.

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Background. Untreated maternal mental health disorders can have devastating sequelae for the mother and child. For women who are currently or planning to become pregnant or are breastfeeding, a critical question is whether the benefits of treating psychiatric illness with pharmacologic interventions outweigh the harms for mother and child. Methods. We conducted a systematic review to assess the benefits and harms of pharmacologic interventions compared with placebo, no treatment, or other pharmacologic interventions for pregnant and postpartum women with mental health disorders. We searched four databases and other sources for evidence available from inception through June 5, 2020 and surveilled the literature through March 2, 2021; dually screened the results; and analyzed eligible studies. We included studies of pregnant, postpartum, or reproductive-age women with a new or preexisting diagnosis of a mental health disorder treated with pharmacotherapy; we excluded psychotherapy. Eligible comparators included women with the disorder but no pharmacotherapy or women who discontinued the pharmacotherapy before pregnancy. Results. A total of 164 studies (168 articles) met eligibility criteria. Brexanolone for depression onset in the third trimester or in the postpartum period probably improves depressive symptoms at 30 days (least square mean difference in the Hamilton Rating Scale for Depression, -2.6; p=0.02; N=209) when compared with placebo. Sertraline for postpartum depression may improve response (calculated relative risk [RR], 2.24; 95% confidence interval [CI], 0.95 to 5.24; N=36), remission (calculated RR, 2.51; 95% CI, 0.94 to 6.70; N=36), and depressive symptoms (p-values ranging from 0.01 to 0.05) when compared with placebo. Discontinuing use of mood stabilizers during pregnancy may increase recurrence (adjusted hazard ratio [AHR], 2.2; 95% CI, 1.2 to 4.2; N=89) and reduce time to recurrence of mood disorders (2 vs. 28 weeks, AHR, 12.1; 95% CI, 1.6 to 91; N=26) for bipolar disorder when compared with continued use. Brexanolone for depression onset in the third trimester or in the postpartum period may increase the risk of sedation or somnolence, leading to dose interruption or reduction when compared with placebo (5% vs. 0%). More than 95 percent of studies reporting on harms were observational in design and unable to fully account for confounding. These studies suggested some associations between benzodiazepine exposure before conception and ectopic pregnancy; between specific antidepressants during pregnancy and adverse maternal outcomes such as postpartum hemorrhage, preeclampsia, and spontaneous abortion, and child outcomes such as respiratory issues, low Apgar scores, persistent pulmonary hypertension of the newborn, depression in children, and autism spectrum disorder; between quetiapine or olanzapine and gestational diabetes; and between benzodiazepine and neonatal intensive care admissions. Causality cannot be inferred from these studies. We found insufficient evidence on benefits and harms from comparative effectiveness studies, with one exception: one study suggested a higher risk of overall congenital anomalies (adjusted RR [ARR], 1.85; 95% CI, 1.23 to 2.78; N=2,608) and cardiac anomalies (ARR, 2.25; 95% CI, 1.17 to 4.34; N=2,608) for lithium compared with lamotrigine during first- trimester exposure. Conclusions. Few studies have been conducted in pregnant and postpartum women on the benefits of pharmacotherapy; many studies report on harms but are of low quality. The limited evidence available is consistent with some benefit, and some studies suggested increased adverse events. However, because these studies could not rule out underlying disease severity as the cause of the association, the causal link between the exposure and adverse events is unclear. Patients and clinicians need to make an informed, collaborative decision on treatment choices.

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