Evidence map›Paper›PMID 25546714›Full record

ArticleClinical toxicology (Philadelphia, Pa.)2015

High-dose hydroxocobalamin administered after H2S exposure counteracts sulfide-poisoning-induced cardiac depression in sheep.

Philippe Haouzi, Bruno Chenuel, Takashi Sonobe

Open access · greenAbstract read
In one paragraph

Article in Clinical toxicology (Philadelphia, Pa.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. 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
  7. Article
  8. Article
  9. Review
  10. Hydrogen Sulfide Toxicity: Mechanism of Action, Clinical Presentation, and Countermeasure Development.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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
  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

3 authors at 2 institutions in 2 countries.

Philippe HaouziDivision of Pulmonary and Critical Medicine, Pennsylvania State University College of Medicine , Hershey, PA , USA.
Bruno Chenuel
Takashi Sonobe
Pennsylvania State University · USUniversité de Lorraine · FR

Funding

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 5R21NS080788-02NINDS NIH HHS R21 NS080788
6 · The paper itself

Abstract

contextSevere H2S poisoning leads to death by rapid respiratory and cardiac arrest, the latter can occur within seconds or minutes in severe forms of intoxication.

objectivesTo determine the time course and the nature of H2S-induced cardiac arrest and the effects of high-dose hydroxocobalamin administered after the end of sulfide exposure. MATERIALS AND

methodsNaHS was infused in 16 sedated mechanically ventilated sheep to reach concentrations of H2S in the blood, which was previously found to lead to cardiac arrest within minutes following the cessation of H2S exposure. High-dose hydroxocobalamin (5 g) or saline solution was administered intravenously, 1 min after the cessation of NaHS infusion.

resultsAll animals were still alive at the cessation of H2S exposure. Three animals (18%) presented a cardiac arrest within 90 s and were unable to receive any antidote or vehicle. In the animals that survived long enough to receive either hydroxocobalamin or saline, 71% (5/7) died in the control group by cardiac arrest within 10 min. In all instances, cardiac arrest was the result of a pulseless electrical activity (PEA). In the group that received the antidote, intravenous injection of 5 g of hydroxocobalamin provoked an abrupt increase in blood pressure and blood flow; PEA was prevented in all instances. However, we could not find any evidence for a recovery in oxidative metabolism in the group receiving hydroxocobalamin, as blood lactate remained elevated and even continued to rise after 1 h, despite restored hemodynamics. This, along with an unaltered recovery of H2S kinetics, suggests that hydroxocobalamin did not act through a mechanism of H2S trapping.

conclusionIn this sheep model, there was a high risk for cardiac arrest, by PEA, persisting up to 10 min after H2S exposure. Very high dose of hydroxocobalamin (5 g), injected very early after the cessation of H2S exposure, improved cardiac contractility and prevented PEA.

Indexed as

AnimalsBlood PressureDisease Models, AnimalHeart ArrestHemodynamicsHydrogen SulfideHydroxocobalaminInjections, IntravenousSheepHydrogen SulfideHydroxocobalaminantidotesCardiac contractilityH2S

Identifiers

PMID25546714
PMCPMC4332828
OpenAlexW2085094537

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Registered trials

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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.