Evidence map›Paper›PMID 14978205›Full record

ArticleThe Journal of physiology2004

Quantitative analysis of cardiovascular modulation in respiratory neural activity.

Thomas E Dick, Kendall F Morris

Abstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Computational models of the neural control of breathing.Wiley interdisciplinary reviews. Systems biology and medicine · 2017
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Pontine mechanisms of respiratory control.Comprehensive Physiology · 2012
    Review
  16. Cardio-ventilatory coupling in young healthy resting subjects.Journal of applied physiology (Bethesda, Md. : 1985) · 2012
    Article
  17. Article
  18. Article
  19. 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

2 authors.

Thomas E DickDepartment of Medicine, University Hospitals Research Institute, Case Western Reserve University, Cleveland, OH 44106-4941, USA. ted3@po.cwru.edu
Kendall F Morris

Funding

BRAINSTEM RESPIRATORY NEURON INTERACTIONSR01NS019814 · NINDS · UNIVERSITY OF SOUTH FLORIDA · PI LINDSEY, BRUCE G · 1985 to 2015
$3.6M
Brainstem Respiratory Neuron InteractionsR37NS019814 · NINDS · UNIVERSITY OF SOUTH FLORIDA · PI LINDSEY, BRUCE G · 2004 to 2010
$3.6M
CONTROL-RESPIRATORY MODULATION OF SYMPATHETIC ACTIVITYR01HL063042 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI DICK, THOMAS E · 2000 to 2003
$911k
BRAINSTEM NEURAL NETWORKS AND AIRWAY DEFENSIVE REFLEXESR01HL049813 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI SHANNON, ROGER · 1994 to 2002
$722k
NHLBI NIH HHS HL-49813NHLBI NIH HHS HL-63042NHLBI NIH HHS R01 HL063042NINDS NIH HHS NS-19814NINDS NIH HHS R01 NS019814NINDS NIH HHS R37 NS019814
6 · The paper itself

Abstract

We propose the 'delta(2)-statistic' for assessing the magnitude and statistical significance of arterial pulse-modulated activity of single neurones and present the results of applying this tool to medullary respiratory-modulated units. This analytical tool is a modification of the eta(2)-statistic and, consequently, based on the analysis of variance. The eta(2)-statistic reflects the consistency of respiratory-modulated activity on a cycle-by-cycle basis. However, directly applying this test to activity during the cardiac cycle proved ineffective because subjects-by-treatments matrices did not contain enough 'information'. We increased information by dividing the cardiac cycle into fewer bins, excluding cycles without activity and summing activity over multiple cycles. The analysed neuronal activity was an existing data set examining the neural control of respiration and cough. Neurones were recorded in the nuclei of the solitary tracts, and in the rostral and caudal ventral respiratory groups of decerebrate, neuromuscularly blocked, ventilated cats (n= 19). Two hundred of 246 spike trains were respiratory modulated; of these 53% were inspiratory (I), 36.5% expiratory (E), 6% IE phase spanning and 4.5% EI phase spanning and responsive to airway stimulation. Nearly half (n= 96/200) of the respiratory-modulated units were significantly pulse modulated and 13 were highly modulated with delta(2) values exceeding 0.3. In 10 of these highly modulated units, eta(2) values were greater than 0.3 and all 13 had, at least, a portion of their activity during expiration. We conclude that cardiorespiratory interaction is reciprocal; in addition to respiratory-modulated activity in a subset of neuronal activity patterns controlling the cardiovascular system, pulse-modulated activity exists in a subset of neuronal activity patterns controlling the respiratory system. Thus, cardio-ventilatory coupling apparent in respiratory motor output is evident and, perhaps, derived from the neural substrate driving that output.

Indexed as

Cardiovascular Physiological PhenomenaRespiratory Physiological PhenomenaAction PotentialsAnalysis of VarianceAnimalsBlood PressureCatsData Interpretation, StatisticalDecerebrate StateFemaleMaleMedulla OblongataPhrenic NervePulseRespiratory System

Identifiers

PMID14978205
PMCPMC1664997

What OpenQuestion holds

Textmetadata
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.