Evidence map›Paper›PMID 34359883›Full record

ReviewCells2021

Brain Protection after Anoxic Brain Injury: Is Lactate Supplementation Helpful?

Filippo Annoni, Lorenzo Peluso, Elisa Gouvêa Bogossian, Jacques Creteur, Elisa R Zanier, Fabio Silvio Taccone

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 2 institutions in 2 countries.

Filippo AnnoniDepartment of Intensive Care, Erasme Hospital, Free University of Brussels, Route de Lennik 808, 1070 Anderlecht, Belgium.ORCID 0000-0002-1271-9034
Lorenzo PelusoDepartment of Intensive Care, Erasme Hospital, Free University of Brussels, Route de Lennik 808, 1070 Anderlecht, Belgium.ORCID 0000-0001-6885-5353
Elisa Gouvêa BogossianDepartment of Intensive Care, Erasme Hospital, Free University of Brussels, Route de Lennik 808, 1070 Anderlecht, Belgium.ORCID 0000-0002-2062-465X
Jacques CreteurDepartment of Intensive Care, Erasme Hospital, Free University of Brussels, Route de Lennik 808, 1070 Anderlecht, Belgium.
Elisa R ZanierLaboratory of Acute Brain Injury and Therapeutic Strategies, Department of Neuroscience, Mario Negri Institute for Pharmacological Research IRCCS, Via Mario Negri 2, 20156 Milan, Italy.ORCID 0000-0002-3011-8718
Fabio Silvio TacconeDepartment of Intensive Care, Erasme Hospital, Free University of Brussels, Route de Lennik 808, 1070 Anderlecht, Belgium.
Erasmus Hospital · BEMario Negri Institute for Pharmacological Research · IT

Funding

Fonds Erasme pour la recherche médicale bouse Chloé
6 · The paper itself

Abstract

While sudden loss of perfusion is responsible for ischemia, failure to supply the required amount of oxygen to the tissues is defined as hypoxia. Among several pathological conditions that can impair brain perfusion and oxygenation, cardiocirculatory arrest is characterized by a complete loss of perfusion to the brain, determining a whole brain ischemic-anoxic injury. Differently from other threatening situations of reduced cerebral perfusion, i.e., caused by increased intracranial pressure or circulatory shock, resuscitated patients after a cardiac arrest experience a sudden restoration of cerebral blood flow and are exposed to a massive reperfusion injury, which could significantly alter cellular metabolism. Current evidence suggests that cell populations in the central nervous system might use alternative metabolic pathways to glucose and that neurons may rely on a lactate-centered metabolism. Indeed, lactate does not require adenosine triphosphate (ATP) to be oxidated and it could therefore serve as an alternative substrate in condition of depleted energy reserves, i.e., reperfusion injury, even in presence of adequate tissue oxygen delivery. Lactate enriched solutions were studied in recent years in healthy subjects, acute heart failure, and severe traumatic brain injured patients, showing possible benefits that extend beyond the role as alternative energetic substrates. In this manuscript, we addressed some key aspects of the cellular metabolic derangements occurring after cerebral ischemia-reperfusion injury and examined the possible rationale for the administration of lactate enriched solutions in resuscitated patients after cardiac arrest.

Indexed as

AcidosisAnimalsBrain Injuries, TraumaticCell DeathCerebrovascular CirculationEnergy MetabolismHeart ArrestHumansHypertonic SolutionsHypoxia-Ischemia, BrainLactic AcidNeuronsNeuroprotective AgentsOxidative StressReperfusion InjuryResuscitationHypertonic SolutionsLactic AcidNeuroprotective Agentscardiac arresthypertonic lactateischemia-reperfusion injuryresuscitation

Identifiers

PMID34359883
PMCPMC8305209
OpenAlexW3180912424

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.