Evidence map›Paper›PMID 25888155›Full record

ReviewCurrent opinion in pediatrics2015

Red cell physiology and signaling relevant to the critical care setting.

Ahmed Said, Stephen Rogers, Allan Doctor

Abstract readReview
In one paragraph

Review in Current opinion in pediatrics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Specific Etiologies Associated With the Multiple Organ Dysfunction Syndrome in Children: Part 2.Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies · 2017
    Review
  6. RBC Distribution Width: Biomarker for Red Cell Dysfunction and Critical Illness Outcome?Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies · 2017
    Observational
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

3 authors.

Ahmed SaidaDepartment of Pediatrics, Division of Critical Care Medicine bDepartment of Biochemistry and Molecular Biophysics, School of Medicine, Washington University in Saint Louis, St. Louis, Missouri, USA.
Stephen Rogers
Allan Doctor

Funding

Washington University Institute of Clinical and Translational Sciences (UL1)UL1RR024992 · NCRR · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2007 to 2011
$45.4M
Washington University Institute of Clinical and Translational SciencesUL1TR000448 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$41.4M
SEPSIS-INDUCED RED CELL DYSFUNCTION (SIRD)R01GM113838 · NIGMS · WASHINGTON UNIVERSITY · PI DOCTOR, ALLAN, MARSHALL, GARLAND ROSS · 2015 to 2019
$4.0M
NCATS NIH HHS UL1 TR000448NCRR NIH HHS UL1 RR024992NIGMS NIH HHS 1R01GM113838-01NIGMS NIH HHS R01 GM113838
6 · The paper itself

Abstract

purpose of reviewOxygen (O2) delivery, the maintenance of which is fundamental to supporting those with critical illness, is a function of blood O2 content and flow. Here, we review red blood cell (RBC) physiology relevant to disordered O2 delivery in the critically ill. RECENT

findingsFlow (rather than content) is the focus of O2 delivery regulation. O2 content is relatively fixed, whereas flow fluctuates by several orders of magnitude. Thus, blood flow volume and distribution vary to maintain coupling between O2 delivery and demand. The trapping, processing and delivery of nitric oxide (NO) by RBCs has emerged as a conserved mechanism through which regional blood flow is linked to biochemical cues of perfusion sufficiency. We will review conventional RBC physiology that influences O2 delivery (O2 affinity & rheology) and introduce a new paradigm for O2 delivery homeostasis based on coordinated gas transport and vascular signaling by RBCs. SUMMARY: By coordinating vascular signaling in a fashion that links O2 and NO flux, RBCs couple vessel caliber (and thus blood flow) to O2 need in tissue. Malfunction of this signaling system is implicated in a wide array of pathophysiologies and may be explanatory for the dysoxia frequently encountered in the critical care setting.

Indexed as

Adaptation, PhysiologicalBiological TransportChildCritical CareCritical IllnessEndothelium, VascularErythrocytesHomeostasisHumansMicrocirculationNitric OxideOxygenPerfusionSignal TransductionNitric OxideOxygen

Identifiers

PMID25888155
PMCPMC4617548

What OpenQuestion holds

Textmetadata
LicenceTDM
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.