Trial reportCritical care (London, England)2009
Pulmonary vascular permeability changes in an ovine model of methicillin-resistant Staphylococcus aureus sepsis.
Trial report in Critical care (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 19 citations in OpenAlex.
- Endothelial dysfunction and immunothrombosis in sepsis.Frontiers in immunology · 2023Review
- Effects of ulinastatin on renal perfusion evaluated by Doppler ultrasonography in a porcine model of septic shock.Experimental and therapeutic medicine · 2021Article
- Monophosphoryl Lipid a Attenuates Multiorgan Dysfunction During Post-Burn Pseudomonas Aeruginosa Pneumonia in Sheep.Shock (Augusta, Ga.) · 2020Article
- Pressure-dependent NOS activation contributes to endothelial hyperpermeability in a model of acute heart failure.Bioscience reports · 2018Article
- A Novel Porcine Model of Septic Shock Induced by Acute Respiratory Distress Syndrome due to Methicillin-resistantChinese medical journal · 2017Article
- SIRT1 protects rat lung tissue against severe burn-induced remote ALI by attenuating the apoptosis of PMVECs via p38 MAPK signaling.Scientific reports · 2015Article
- Dusp3 and Psme3 are associated with murine susceptibility to Staphylococcus aureus infection and human sepsis.PLoS pathogens · 2014Article
- Hypoxia-inducible factor 1-regulated lysyl oxidase is involved in Staphylococcus aureus abscess formation.Infection and immunity · 2013Article
- Pulmonary microvascular hyperpermeability and expression of vascular endothelial growth factor in smoke inhalation- and pneumonia-induced acute lung injury.Burns : journal of the International Society for Burn Injuries · 2012Article
- Dopamine inhibits pulmonary edema through the VEGF-VEGFR2 axis in a murine model of acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Pseudomonas aeruginosa is associated with increased lung cytokines and asymmetric dimethylarginine compared with methicillin-resistant Staphylococcus aureus.Shock (Augusta, Ga.) · 2011Article
- Year in review 2009: Critical Care--shock.Critical care (London, England) · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionEndothelial dysfunction is a hallmark of sepsis, associated with lung transvascular fluid flux and pulmonary dysfunction in septic patients. We tested the hypothesis that methicillin-resistant Staphylococcus aureus (MRSA) sepsis following smoke inhalation increases pulmonary transvascular fluid flux via excessive nitric oxide (NO) production.
methodsEwes were chronically instrumented, and randomised into either a control or MRSA sepsis (MRSA and smoke inhalation) group.
resultsPulmonary function remained stable in the control group, whereas the MRSA sepsis group developed impaired gas exchange and significantly increased lung lymph flow, permeability index and bloodless wet-to-dry weight-ratio (W/D ratio). The plasma nitrate/nitrite (NOx) levels, lung inducible nitric oxide synthases (iNOS) and endothelial nitric oxide synthases (eNOS), vascular endothelial growth factor (VEGF) protein expressions and poly-(ADP)-ribose (PAR) were significantly increased by MRSA challenge.
conclusionsThese results provide evidence that excessive NO production may mediate pulmonary vascular hyperpermeability in MRSA sepsis via up regulation of reactive radicals and VEGF.
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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.