Evidence map›Paper›PMID 21949154›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

Phosphodiesterase 4 inhibition attenuates persistent heart and lung injury by neonatal hyperoxia in rats.

Yvonne P de Visser, Frans J Walther, El Houari Laghmani, Paul Steendijk, Maaike Middeldorp, Arnoud van der Laarse, Gerry T M Wagenaar

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  5. Interactive and independent effects of early lipopolysaccharide and hyperoxia exposure on developing murine lungs.American journal of physiology. Lung cellular and molecular physiology · 2020
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  18. Metformin attenuates hyperoxia-induced lung injury in neonatal rats by reducing the inflammatory response.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Yvonne P de VisserDepartment of Pediatrics, Division of Neonatology, Leiden University Medical Center, Leiden, the Netherlands.
Frans J Walther
El Houari Laghmani
Paul Steendijk
Maaike Middeldorp
Arnoud van der Laarse
Gerry T M Wagenaar
Pediatrics and Genetics · USLeiden University Medical Center · NLThe Lundquist Institute · US

Funding

Synthetic Lung Surfactant Optimized for Biomedical ApplicationR01HL092158 · NHLBI · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI WALTHER, FRANCISKUS JOHANNES · 2008 to 2011
$1.3M
Synthetic surfactant and toxic chemical lung injuryR01ES015330 · NIEHS · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI WALTHER, FRANCISKUS JOHANNES · 2008 to 2011
$1.2M
NHLBI NIH HHS 1R01 HL092158NHLBI NIH HHS R01 HL092158NIEHS NIH HHS 1R01 ES015330NIEHS NIH HHS R01 ES015330
6 · The paper itself

Abstract

Phosphodiesterase (PDE) 4 inhibitors are potent anti-inflammatory drugs with antihypertensive properties, and their therapeutic role in bronchopulmonary dysplasia (BPD) is still controversial. We studied the role of PDE4 inhibition with piclamilast on normal lung development and its therapeutic value on pulmonary hypertension (PH) and right ventricular hypertrophy (RVH) in neonatal rats with hyperoxia-induced lung injury, a valuable model for premature infants with severe BPD. The cardiopulmonary effects of piclamilast treatment (5 mg·kg(-1)·day(-1)) were investigated in two models of experimental BPD: 1) daily treatment during continuous exposure to hyperoxia for 10 days; and 2) late treatment and injury-recovery in which pups were exposed to hyperoxia or room air for 9 days, followed by 9 or 42 days of recovery in room air combined with treatment started on day 6 of oxygen exposure until day 18. Prophylactic piclamilast treatment reduced pulmonary fibrin deposition, septum thickness, arteriolar wall thickness, arteriolar vascular smooth muscle cell proliferation and RVH, and prolonged survival. In the late treatment and injury-recovery model, hyperoxia caused persistent aberrant alveolar and vascular development, PH, and RVH. Treatment with piclamilast in both models reduced arteriolar wall thickness, attenuated RVH, and improved right ventricular function in the injury recovery model, but did not restore alveolarization or angiogenesis. Treatment with piclamilast did not show adverse cardiopulmonary effects in room air controls in both models. In conclusion, PDE4 inhibition attenuated and partially reversed PH and RVH, but did not advance alveolar development in neonatal rats with hyperoxic lung injury or affect normal lung and heart development.

Indexed as

BenzamidesBronchopulmonary DysplasiaPhosphodiesterase 4 InhibitorsPyridinesAnimalsAnimals, NewbornCyclic Nucleotide Phosphodiesterases, Type 4Disease Models, AnimalHeartHeart InjuriesHumansHyperoxiaHypertension, PulmonaryHypertrophy, Right VentricularInfant, NewbornLungBenzamidesCyclic Nucleotide Phosphodiesterases, Type 4OxygenPhosphodiesterase 4 InhibitorspiclamilastPyridines

Identifiers

PMID21949154
PMCPMC3349366
OpenAlexW2049682114

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.