Evidence map›Paper›PMID 17434976›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2007

Increased cardiac sympathetic nerve activity in heart failure is not due to desensitization of the arterial baroreflex.

A M D Watson, S G Hood, R Ramchandra, R M McAllen, C N May

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PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Guidelines for rigor and reproducibility of heart rate variability within human cardiovascular research.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
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  11. Nonpharmacological Correction of Hypersympatheticotonia in Patients with Chronic Coronary Insufficiency and Severe Left Ventricular Dysfunction.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2016
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Intracarotid hypertonic sodium chloride differentially modulates sympathetic nerve activity to the heart and kidney.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    Article
  17. Review
  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

5 authors at 1 institution in 1 country.

A M D WatsonHoward Florey Institute, University of Melbourne, Parkville, Victoria 3010, Australia.
S G Hood
R Ramchandra
R M McAllen
C N May
University of Melbourne · AU

Funding

Cardiac sympathetic drive mechanism in heart failureR01HL074932 · NHLBI · UNIVERSITY OF MELBOURNE · PI MAY, CLIVE N · 2004 to 2007
$785k
NHLBI NIH HHS 5R01 HL 74932NHLBI NIH HHS R01 HL074932
6 · The paper itself

Abstract

Increased sympathetic drive to the heart worsens prognosis in heart failure, but the level of cardiac sympathetic nerve activity (CSNA) has been assessed only by indirect methods, which do not permit testing of whether its control by arterial baroreceptors is defective. To do this, CSNA was measured directly in 16 female sheep, 8 of which had been ventricularly paced at 200-220 beats/min for 4-6 wk, until their ejection fraction fell to between 35 and 40%. Recording electrodes were surgically implanted in the cardiac sympathetic nerves, and after 3 days' recovery the responses to intravenous phenylephrine and nitroprusside infusions were measured in conscious sheep. Electrophysiological recordings showed that resting CSNA (bursts/100 heartbeats) was significantly elevated in heart-failure sheep (89 +/- 3) compared with normal animals (46 +/- 6; P < 0.001). This increased CSNA was not accompanied by any increase in the low-frequency power of heart-rate variability. The baroreceptor-heart rate reflex was significantly depressed in heart failure (maximum gain -3.29 +/- 0.56 vs. -5.34 +/- 0.66 beats.min(-1).mmHg(-1) in normal animals), confirming published findings. In contrast, the baroreflex control of CSNA was undiminished (maximum gain in heart failure -6.33 +/- 1.06 vs. -6.03 +/- 0.95%max/mmHg in normal sheep). Direct recordings in a sheep model of heart failure thus show that resting CSNA is strikingly increased, but this is not due to defective control by arterial baroreceptors.

Indexed as

BaroreflexBlood PressureHeart RateAnimalsArteriesCardiac Output, LowFemaleSheepSympathetic Nervous System

Identifiers

PMID17434976
PMCPMC2084464
OpenAlexW2117644546

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.