Evidence map›Paper›PMID 25616319›Full record

ArticleCardiovascular toxicology2016

Sulfide Intoxication-Induced Circulatory Failure is Mediated by a Depression in Cardiac Contractility.

Takashi Sonobe, Philippe Haouzi

Abstract read
In one paragraph

Article in Cardiovascular toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A Sulfonyl Azide-Based Sulfide Scavenger Rescues Mice from Lethal Hydrogen Sulfide Intoxication.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  5. Review
  6. Antidotal Effects of the Phenothiazine Chromophore Methylene Blue Following Cyanide Intoxication.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
  7. Oxidative Stress Effects of Soluble Sulfide on Human Hepatocyte Cell Line LO2.International journal of environmental research and public health · 2019
    Article
  8. Article
  9. Article
  10. Methylene Blue Counteracts HCardiovascular toxicology · 2018
    Article
  11. Total Flavones ofEvidence-based complementary and alternative medicine : eCAM · 2018
    Article
  12. Article
  13. Article
  14. Review
  15. Methylene blue counteracts H2S toxicity-induced cardiac depression by restoring L-type Ca channel activity.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  16. Review
  17. Article
  18. Article
  19. 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 at 1 institution in 1 country.

Takashi SonobeDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Pennsylvania State University, College of Medicine, 500 University Drive, H041, Hershey, PA, 17033, USA.
Philippe HaouziDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Pennsylvania State University, College of Medicine, 500 University Drive, H041, Hershey, PA, 17033, USA. phaouzi@hmc.psu.edu.
Pennsylvania State University · US

Funding

Methylene Blue, A Novel Treatment of H2S Poisoning-induced Brain InjuryR21NS090017 · NINDS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI HAOUZI, PHILIPPE A · 2014 to 2015
$802k
Crystalline hydroxocobalamin and methemoglobin as a treatment of H2S intoxicationR21NS080788 · NINDS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI HAOUZI, PHILIPPE A · 2012 to 2013
$752k
NINDS NIH HHS 1R21NS080788-01NINDS NIH HHS 1R21NS090017-01NINDS NIH HHS R21 NS080788NINDS NIH HHS R21 NS090017
6 · The paper itself

Abstract

Hydrogen sulfide (H2S) intoxication produces a rapid cardio-circulatory failure leading to cardiac arrest. In non-lethal forms of sulfide exposure, the presence of a circulatory shock is associated with long-term neurological sequelae. Our aim was to clarify the mechanisms of H2S-induced circulatory failure. In anesthetized, paralyzed, and mechanically ventilated rats, cardiac output, arterial pressure and ventricular pressures were determined while NaHS was infused to increase arterial concentration of soluble H2S (CgH2S) from undetectable to levels leading to circulatory failure. Compared to control/saline infusion, blood pressure started to decrease significantly along with a modest drop in peripheral vascular resistance (-19 ± 5%, P < 0.01), when CgH2S reached about 1 μM. As CgH2S exceeded 2-3 μM, parameters of ventricular contractility diminished with no further reduction in peripheral resistance. Whenever H2S exposure was maintained at a higher level (CgH2S over 7 μM), a severe depression of cardiac contractility was observed, leading to asystole within minutes, but with no evidence of peripheral vasoplegia. The immediate and long-term neurological effects of specifically counteracting sulfide-induced cardiac contractility depression following H2S exposure remain to be investigated.

Indexed as

Air PollutantsAnesthesiaAnimalsArterial PressureBlood Gas AnalysisCardiac OutputHeart VentriclesHydrogen SulfideLactic AcidMaleMyocardial ContractionRatsRats, Sprague-DawleyShockVascular ResistanceVasoplegiaAir PollutantsHydrogen SulfideLactic AcidCardiac toxicityH2SVascular blood flowVasodilation

Identifiers

PMID25616319
PMCPMC4514577
OpenAlexW2079710697

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.