Evidence map›Paper›PMID 22069736›Full record

ArticleToxins2011

Hemodynamic effects of anthrax toxins in the rabbit model and the cardiac pathology induced by lethal toxin.

William S Lawrence, Jeffrey R Marshall, Diana L Zavala, Lori E Weaver, Wallace B Baze, Scott T Moen, Elbert B Whorton, Randy L Gourley, Johnny W Peterson

Open access · goldAbstract read
In one paragraph

Article in Toxins, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. American journal of physiology. Heart and circulatory physiology · 2019
    Article
  4. Small molecule inhibitors of anthrax edema factor.Bioorganic & medicinal chemistry letters · 2018
    Article
  5. Using Telemetry Data to Refine Endpoints for New Zealand White Rabbits Challenged withJournal of the American Association for Laboratory Animal Science : JAALAS · 2017
    Article
  6. Review
  7. Article
  8. Molecular determinants for a cardiovascular collapse in anthrax.Frontiers in bioscience (Elite edition) · 2014
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. 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

9 authors at 2 institutions in 1 country.

William S LawrenceDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston/TX 77555, USA. wslawren@utmb.edu
Jeffrey R Marshall
Diana L Zavala
Lori E Weaver
Wallace B Baze
Scott T Moen
Elbert B Whorton
Randy L Gourley
Johnny W Peterson
The University of Texas Medical Branch at Galveston · USThe University of Texas MD Anderson Cancer Center · US

Funding

NIAID NIH HHS N01 AI030065NIAID NIH HHS N01-AI-30065
6 · The paper itself

Abstract

Anthrax lethal toxin (LeTx) and edema toxin (EdTx) have been shown to alter hemodynamics in the rodent model, while LeTx primarily is reported to induce extensive tissue pathology. However, the rodent model has limitations when used for comparison to higher organisms such as humans. The rabbit model, on the other hand, has gained recognition as a useful model for studying anthrax infection and its pathophysiological effects. In this study, we assessed the hemodynamic effects of lethal toxin (LeTx) and edema toxin (EdTx) in the rabbit model using physiologically relevant amounts of the toxins. Moreover, we further examine the pathological effects of LeTx on cardiac tissue. We intravenously injected Dutch-belted rabbits with either low-dose and high-dose recombinant LeTx or a single dose of EdTx. The animals' heart rate and mean arterial pressure were continuously monitored via telemetry until either 48 or 72 h post-challenge. Additional animals challenged with LeTx were used for cardiac troponin I (cTnI) quantitation, cardiac histopathology, and echocardiography. LeTx depressed heart rate at the lower dose and mean arterial pressure (MAP) at the higher dose. EdTx, on the other hand, temporarily intensified heart rate while lowering MAP. Both doses of LeTx caused cardiac pathology with the higher dose having a more profound effect. Lastly, left-ventricular dilation due to LeTx was not apparent at the given time-points. Our study demonstrates the hemodynamic effects of anthrax toxins, as well as the pathological effects of LeTx on the heart in the rabbit model, and it provides further evidence for the toxins' direct impact on the heart.

Indexed as

AnimalsAntigens, BacterialBacterial ToxinsBlood PressureDose-Response Relationship, DrugEchocardiographyFemaleHeart RateMyocardiumRabbitsTelemetryTroponin Ianthrax toxinAntigens, BacterialBacterial ToxinsTroponin Ianthraxcardiaclethal toxinrabbit model

Identifiers

PMID22069736
PMCPMC3202836
OpenAlexW2117111287

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.