Evidence map›Paper›PMID 34848804›Full record

ArticleScientific reports2021

Comparative effects of dexmedetomidine and propofol on brain and lung damage in experimental acute ischemic stroke.

Giselle C Sousa, Marcos Vinicius Fernandes, Fernanda F Cruz, Mariana A Antunes, Carla M da Silva, Christina Takyia, Denise Battaglini, Cynthia S Samary, Chiara Robba, Paolo Pelosi and 2 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.

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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

12 authors at 4 institutions in 2 countries.

Giselle C SousaLaboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Marcos Vinicius FernandesLaboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Fernanda F CruzLaboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Mariana A AntunesLaboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Carla M da SilvaLaboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Christina TakyiaLaboratory of Imunopathology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Denise BattagliniSan Martino Policlinico Hospital, IRCCS for Oncology and Neurosciences, University of Genoa, Genoa, Italy.
Cynthia S SamaryLaboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Chiara RobbaSan Martino Policlinico Hospital, IRCCS for Oncology and Neurosciences, University of Genoa, Genoa, Italy.
Paolo PelosiSan Martino Policlinico Hospital, IRCCS for Oncology and Neurosciences, University of Genoa, Genoa, Italy.
Patricia R M Rocco *Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Pedro L Silva *Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil. pedroleme@biof.ufrj.br.
Universidade Federal do Rio de Janeiro · BRFundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro · BROspedale Policlinico San Martino · ITUniversity of Genoa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute ischemic stroke is associated with pulmonary complications, and often dexmedetomidine and propofol are used to decrease cerebral metabolic rate. However, it is unknown the immunomodulatory actions of dexmedetomidine and propofol on brain and lungs during acute ischemic stroke. The effects of dexmedetomidine and propofol were compared on perilesional brain tissue and lung damage after acute ischemic stroke in rats. Further, the mean amount of both sedatives was directly evaluated on alveolar macrophages and lung endothelial cells primarily extracted 24-h after acute ischemic stroke. In twenty-five Wistar rats, ischemic stroke was induced and after 24-h treated with sodium thiopental (STROKE), dexmedetomidine and propofol. Dexmedetomidine, compared to STROKE, reduced diffuse alveolar damage score [median(interquartile range); 12(7.8-15.3) vs. 19.5(18-24), p = 0.007)], bronchoconstriction index [2.28(2.08-2.36) vs. 2.64(2.53-2.77), p = 0.006], and TNF-α expression (p = 0.0003), while propofol increased VCAM-1 expression compared to STROKE (p = 0.0004). In perilesional brain tissue, dexmedetomidine, compared to STROKE, decreased TNF-α (p = 0.010), while propofol increased VCAM-1 compared to STROKE (p = 0.024). In alveolar macrophages and endothelial cells, dexmedetomidine decreased IL-6 and IL-1β compared to STROKE (p = 0.002, and p = 0.040, respectively), and reduced IL-1β compared to propofol (p = 0.014). Dexmedetomidine, but not propofol, induced brain and lung protection in experimental acute ischemic stroke.

Indexed as

AnimalsBrainBrain IschemiaDexmedetomidineDisease Models, AnimalEndothelial CellsHypnotics and SedativesInterleukin-1betaInterleukin-6Ischemic StrokeLungMacrophages, AlveolarMalePropofolRatsRats, WistarDexmedetomidineHypnotics and SedativesIL1B protein, ratIl6 protein, ratInterleukin-1betaInterleukin-6PropofolThiopentalTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID34848804
PMCPMC8633001
OpenAlexW3217210464

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Registered trials

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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.