Evidence map›Paper›PMID 21063241›Full record

ArticleShock (Augusta, Ga.)2011

A physiological model for autonomic heart rate regulation in human endotoxemia.

Panagiota T Foteinou, Steve E Calvano, Stephen F Lowry, Ioannis P Androulakis

Abstract read
In one paragraph

Article in Shock (Augusta, Ga.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Multiscale modeling methods in biomechanics.Wiley interdisciplinary reviews. Systems biology and medicine · 2017
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Modeling physiologic variability in human endotoxemia.Critical reviews in biomedical engineering · 2012
    Article
  20. Article
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

4 authors at 2 institutions in 1 country.

Panagiota T FoteinouBiomedical Engineering, Rutgers University, Piscataway.
Steve E Calvano
Stephen F Lowry
Ioannis P Androulakis
Johnson University · USRutgers, The State University of New Jersey · US

Funding

HORMONE AND CYTOKINE REGULATION OF ENDOTOXIN INJURY(RMI)R37GM034695 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI LOWRY, STEPHEN F · 1997 to 2006
$4.0M
SKELETAL MUSCLE PROTEIN RESPONSE TO INJURY AND REPLETIONR01GM034695 · NIGMS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI CORBETT, SIOBHAN A · 1985 to 2011
$2.8M
Bioinformatics Analysis of Control Mechanisms of HypermetabolismR01GM082974 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI ANDROULAKIS, IOANNIS P · 2008 to 2011
$1.6M
NIGMS NIH HHS GM082974NIGMS NIH HHS GM34695NIGMS NIH HHS R01 GM034695NIGMS NIH HHS R01 GM082974NIGMS NIH HHS R37 GM034695
6 · The paper itself

Abstract

The systemic inflammatory response syndrome often accompanies critical illnesses and can be an important cause of morbidity and mortality. Marked abnormalities in cardiovascular function accompany acute illnesses manifested as sustained tachyarrhythmias, which are but one component of systemic dysregulation. The realization that cardiac pacemaker activity is under control of the autonomic nervous system has promoted the analysis of heart rate (HR) variation for assessing autonomic activities. In acute illnesses, autonomic imbalance manifesting in part as parasympathetic attenuation is associated with increased morbidity in patients who manifest systemic inflammatory response syndrome phenotype. Driven by the premise that biological phenotypes emerge as the outcome of the coordinated action of network elements across the host, a multiscale model of human endotoxemia, as a prototype model of systemic inflammation in humans, is developed that quantifies critical aspects of the complex relationship between inflammation and autonomic HR regulation. In the present study, changes in HR response to acute injury, phenotypically expressed as tachycardia, are simulated as a result of autonomic imbalance that reflects sympathetic activity excess and parasympathetic attenuation. The proposed model assesses both the anti-inflammatory and cardiovascular effects of antecedent stresses upon the systemic inflammatory manifestations of human endotoxemia as well as a series of nonlinear inflammatory relevant scenarios. Such a modeling approach provides a comprehensive conceptual framework linking inflammation and physiological complexity via a multiscale model that may advance the translational potential of systems modeling in clinical research.

Indexed as

Models, TheoreticalAutonomic Nervous SystemEndotoxemiaHeart RateHumansSystemic Inflammatory Response SyndromeTachycardia

Identifiers

PMID21063241
PMCPMC3045969
OpenAlexW1979442665

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.