ReviewScientifica2012
Contribution of α - and β -Adrenergic Mechanisms to the Development of Pulmonary Edema.
Review in Scientifica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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.
Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Cardiogenic pulmonary edema - is it lone cardiogenic? "Missing link" between hemodynamic and other existing mechanisms.American journal of cardiovascular disease · 2024Review
- Article
- A comprehensive guide to the pharmacologic regulation of angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 entry receptor.Pharmacology & therapeutics · 2021Review
- Beta-Adrenergic Blockade in Critical Illness.Frontiers in pharmacology · 2021Review
- Beta-Adrenergic Blockers as a Potential Treatment for COVID-19 Patients.BioEssays : news and reviews in molecular, cellular and developmental biology · 2020Article
- Exacerbation of ozone-induced pulmonary and systemic effects by βScientific reports · 2019Article
- Immersion pulmonary oedema: a cardiological perspective.Diving and hyperbaric medicine · 2019Article
- Argon reduces the pulmonary vascular tone in rats and humans by GABA-receptor activation.Scientific reports · 2019Article
- Intraoperative hemodynamics monitoring in a patient with pheochromocytoma multisystem crisis: a case report.JA clinical reports · 2018Article
- Anesthesia for myelomeningocele surgery in fetus.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2017Review
- Pheochromocytoma Multisystem Crisis Behaving Like Interstitial Pneumonia: An Autopsy Case.Internal medicine (Tokyo, Japan) · 2017Article
- Elevated blood plasma levels of epinephrine, norepinephrine, tyrosine hydroxylase, TGFβ1, and TNFα associated with high-altitude pulmonary edema in an Indian population.Therapeutics and clinical risk management · 2016Article
- Acute pulmonary edema following liposuction due to heart failure and atypical pneumonia.Wiener medizinische Wochenschrift (1946) · 2015Article
- Cross-talk between the inflammatory response, sympathetic activation and pulmonary infection in the ischemic stroke.Journal of neuroinflammation · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endogenous or exogenous catecholamines can induce pulmonary edema (PE). This may occur in human pathologic conditions such as in pheochromocytoma or in neurogenic pulmonary edema (NPE) but can also be provoked after experimental administration of adrenergic agonists. PE can result from stimulation with different types of adrenergic stimulation. With α-adrenergic treatment, it develops more rapidly, is more severe with abundant protein-rich fluid in the alveolar space, and is accompanied by strong generalized inflammation in the lung. Similar detrimental effects of α-adrenergic stimulation have repeatedly been described and are considered to play a pivotal role in NPE or in PE in patients with pheochromocytoma. Although β-adrenergic agonists have often been reported to prevent or attenuate PE by enhancing alveolar fluid clearance, PE may also be induced by β-adrenergic treatment as can be observed in tocolysis. In experimental models, infusion of β-adrenergic agonists induces less severe PE than α-adrenergic stimulation. The present paper addresses the current understanding of the possible contribution of α- and β-adrenergic pathways to the development of PE.
Identifiers
What OpenQuestion holds
Registered trials
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.