Recent Advances in the Pathogenesis and Treatment of Persistent Pulmonary Hypertension of the Newborn

Abman, Steven H.

doi:10.1159/000101343

Cited by 111 publications

(128 citation statements)

References 116 publications

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“…Newborns with PPHN are at risk of severe asphyxia and its complications including death, neurologic injury and other problems. Studies over the past two decades have clearly shown the critical role of NO-cGMP signaling in the regulation of the fetal and neonatal pulmonary circulation, and that disruption of the NO-cGMP cascade during the perinatal period leads to PPHN 7) .…”

Section: Persistent Pulmonary Hypertensionmentioning

confidence: 99%

Neonatal respiratory distress: recent progress in understanding pathogenesis and treatment outcomes

Kim

2010

Korean J Pediatr

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= Abstract = Transient tachypnea of the newborn (TTN), respiratory distress syndrome (RDS), and persistent pulmonary hypertension (PPHN) are the three most common disorders that cause respiratory distress after birth. An understanding of the pathophysiology of these disorders and the development of effective therapeutic strategies is required to control these conditions. Here, we review recent papers on the pathogenesis and treatment of neonatal respiratory disease. (

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Section: Persistent Pulmonary Hypertensionmentioning

confidence: 99%

Neonatal respiratory distress: recent progress in understanding pathogenesis and treatment outcomes

Kim

2010

Korean J Pediatr

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“…Since its development, FSD has been used to treat cerebral vasospasms, which may result in subarachnoid hemorrhage and lead to cognitive decline in stroke victims. It also is effective for the treatment of pulmonary hypertension (19). In general, ROCK inhibitors are valid treatment options for ischemic cardiovascular and cerebrovascular diseases (20).…”

Section: Introductionmentioning

confidence: 99%

Effects of a Rho kinase inhibitor on the sequential expression of ICAM-1, HIF-1α, Bcl-2 and caspase-3 in the retina of rats with oxygen-induced retinopathy

Wang

Chen

2013

International Journal of Molecular Medicine

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Abstract. The aim of the present study was to evaluate the effects of blocking the Rho kinase pathway on non-perfused regions and angiogenesis in the retina of rats using a rat model of oxygen-induced retinopathy (OIR) by observing the sequential expression of intercellular adhesion molecule-1 (ICAM-1), hypoxia-inducible factor-1 (HIF-1), B-cell lymphoma/leukemia-2 gene (Bcl-2) and caspase-3 mRNA following the administration of the Rho kinase inhibitor, fasudil (FSD). A total of 240 newborn rats were randomly divided into a normoxia control (N) group, a hyperoxia (H) group and a H + FSD (HF) group. The rats were sacrificed, and the eyes were enucleated from postnatal day (P)12 to P21. Samples were prepared for retinal flat mounts, mRNA and protein quantification. On P14, a higher number of circuitous retinal veins was observed in the H group compared with the HF group. In the HF group, the avascular area was significantly reduced compared with the H group on P18 (P<0.01). In the HF group, the mRNA expression of Bcl-2 was significantly increased on P15 compared with the N and H group (P<0.01). On P15 and P17 in the H group and on P13 in the HF group, the mRNA expression of ICAM-1 was significantly increased compared with the other groups (P<0.05). In the H and HF group, the expression of HIF-1α was significantly increased on P12 compared with the N group (P<0.05). On P19 and P21, HIF-1α expression was significantly increased to a maximum level in the HF group compared with the H and N group (P<0.01). In conclusion, these results suggest that FSD inhibits the expression of ICAM-1, assisting in the release of Bcl-2, suppressing caspase-3. In the HF group, the retinal flat mounts revealed that FSD had a vasorelaxant effect. On P18, a double-layered retinal vascular network was formed, and the number of non-perfused regions was significantly reduced. However, the late-phase peak expression of HIF-1α resulted in an inevitable increase in vascular endothelial growth factor expression and further accelerated neovascularization and vascular reconstruction in the immature retinal model.

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“…Persistent pulmonary hypertension of the newborn (PPHN), which occurs exclusively in the neonatal period, is also classified as PAH according to the Dana Point clinical classification of pulmonary hypertension [10]. However, the epidemiology, natural history, treatment and outcome of PPHN are sufficiently distinct from the chronic, progressive PAH seen in paediatric patients that we have excluded it from the present discussion [11]. Finally, untreated paediatric PAH has been reported to be associated with a median survival of 10 months, which is worse compared with adults (median untreated survival of 2.8 yrs) [12].…”

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confidence: 99%

Treatment options for paediatric pulmonary arterial hypertension

Berger¹,

Bonnet²

2010

Eur Respir Rev

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Pulmonary arterial hypertension (PAH) is a serious, progressive condition, which can present idiopathically or secondary to conditions such as systemic sclerosis or congenital heart disease. The condition exists in both adult and paediatric forms, which possess several similar characteristics. Adult and paediatric PAH can, however, be distinguished based on underlying pathology and the presence of age-specific conditions, some of which are related to poor lung development in children. Improved knowledge of vascular biology has led to the development of several PAH-specific therapies, which have demonstrated clinical benefits in adults, including improved exercise capacity and prolonged survival. Treatment data in paediatric PAH are scarce. Although limited, the existing data indicate that current treatments for paediatric PAH are well tolerated and effective, at least in the short-and medium-term. Nevertheless, the current guidelines for clinicians, which recommend use of the adult treatment algorithm in paediatric patients, appear justified when judged according to the available evidence. However, further randomised, controlled trials are necessary to increase the evidence base for treatment of paediatric PAH, especially in relation to age-specific conditions. At present, early initiation of treatment and combination pharmacological therapy may offer the most promising courses of action to improve outcomes in paediatric PAH.

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Recent Advances in the Pathogenesis and Treatment of Persistent Pulmonary Hypertension of the Newborn

Cited by 111 publications

References 116 publications

Neonatal respiratory distress: recent progress in understanding pathogenesis and treatment outcomes

Neonatal respiratory distress: recent progress in understanding pathogenesis and treatment outcomes

Effects of a Rho kinase inhibitor on the sequential expression of ICAM-1, HIF-1α, Bcl-2 and caspase-3 in the retina of rats with oxygen-induced retinopathy

Treatment options for paediatric pulmonary arterial hypertension

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