Evidence map›Paper›PMID 16886062›Full record

ArticleThe Journal of clinical investigation2006

Anaphylactic shock depends on PI3K and eNOS-derived NO.

Anje Cauwels, Ben Janssen, Emmanuel Buys, Patrick Sips, Peter Brouckaert

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 132 citations in OpenAlex.

  1. Efficacy of Treating Nifedipine-Induced Shock with Hydroxocobalamin in a Swine Model.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2025
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  9. Proteomic and Biological Analysis of anFrontiers in immunology · 2021
    Article
  10. Effects of NO/cGMP inhibitors in a rat model of anaphylactoid shock.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    Article
  11. Article
  12. Change in exhaled nitric oxide during peanut challenge is related to severity of reaction.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2020
    Article
  13. Article
  14. Article
  15. Regulation of vascular permeability in anaphylaxis.British journal of pharmacology · 2018
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 2 countries.

Anje CauwelsMolecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University, Belgium, and Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, USA. Anje.Cauwels@dmbr.UGent.be
Ben Janssen
Emmanuel Buys
Patrick Sips
Peter Brouckaert
Ghent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anaphylactic shock is a sudden, life-threatening allergic reaction associated with severe hypotension. Platelet-activating factor (PAF) is implicated in the cardiovascular dysfunctions occurring in various shock syndromes, including anaphylaxis. Excessive production of the vasodilator NO causes inflammatory hypotension and shock, and it is generally accepted that transcriptionally regulated inducible iNOS is responsible for this. Nevertheless, the contribution of NO to PAF-induced shock or anaphylactic shock is still ambiguous. We studied PAF and anaphylactic shock in conscious mice. Surprisingly, hyperacute PAF shock depended entirely on NO, produced not by inducible iNOS, but by constitutive eNOS, rapidly activated via the PI3K pathway. Soluble guanylate cyclase (sGC) is generally regarded as the principal vasorelaxing mediator of NO. Nevertheless, although methylene blue partially prevented PAF shock, neither 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ) nor sGCalpha1 deficiency did. Also, in 2 different models of active systemic anaphylaxis, inhibition of NOS, PI3K, or Akt or eNOS deficiency provided complete protection. In contrast to the unsubstantiated paradigm that only excessive iNOS-derived NO underlies cardiovascular collapse in shock, our data strongly support the unexpected concept that eNOS-derived NO is the principal vasodilator in anaphylactic shock and define eNOS and/or PI3K or Akt as new potential targets for treating anaphylaxis.

Indexed as

AnaphylaxisAnimalsBlood PressureCardiovascular DiseasesEnzyme InhibitorsMiceMice, Inbred C57BLMice, KnockoutNitric OxideNitric Oxide Synthase Type IIIOxadiazolesPhosphatidylinositol 3-KinasesPlatelet Activating FactorQuinoxalinesSerum Albumin, BovineTranscription, Genetic1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-oneEnzyme InhibitorsNitric OxideNitric Oxide Synthase Type IIIOxadiazolesPhosphatidylinositol 3-KinasesPlatelet Activating FactorQuinoxalinesSerum Albumin, Bovine

Identifiers

PMID16886062
PMCPMC1523420
OpenAlexW2119961921

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.