Evidence map›Paper›PMID 24785379›Full record

ArticleNeurotoxicology2014

Development of status epilepticus, sustained calcium elevations and neuronal injury in a rat survival model of lethal paraoxon intoxication.

Laxmikant S Deshpande, Dawn S Carter, Kristin F Phillips, Robert E Blair, Robert J DeLorenzo

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurotoxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
8.4field-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

31 citing papers in PubMed, 63 citations in OpenAlex.

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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.

Laxmikant S DeshpandeDepartments of Neurology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Dawn S CarterDepartments of Neurology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Kristin F PhillipsDepartments of Neurology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Robert E BlairDepartments of Neurology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Robert J DeLorenzoDepartments of Neurology, Virginia Commonwealth University, Richmond, VA 23298, USA; Departments of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA; Departments of Molecular Biophysics and Biochemistry, Virginia Commonwealth University, Richmond, VA 23298, USA. Electronic address: rdeloren@hsc.vcu.edu.
Virginia Commonwealth University · US

Funding

PARATHION EXPOSURE: MECHANISMS OF TOXICTY AND TREATMENTU01NS058213 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI DELORENZO, ROBERT JOHN · 2006 to 2015
$5.0M
HYPOTHERMIA PROTECTS AGAINST ORGANOPHOSPHATE TOXICITYR21NS072061 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI DELORENZO, ROBERT JOHN · 2011 to 2012
$748k
NINDS NIH HHS R21 NS072061NINDS NIH HHS R21NS072061NINDS NIH HHS U01 NS058213NINDS NIH HHS U01NS058213
6 · The paper itself

Abstract

Paraoxon (POX) is an active metabolite of organophosphate (OP) pesticide parathion that has been weaponized and used against civilian populations. Exposure to POX produces high mortality. OP poisoning is often associated with chronic neurological disorders. In this study, we optimize a rat survival model of lethal POX exposures in order to mimic both acute and long-term effects of POX intoxication. Male Sprague-Dawley rats injected with POX (4mg/kg, ice-cold PBS, s.c.) produced a rapid cholinergic crisis that evolved into status epilepticus (SE) and death within 6-8min. The EEG profile for POX induced SE was characterized and showed clinical and electrographic seizures with 7-10Hz spike activity. Treatment of 100% lethal POX intoxication with an optimized three drug regimen (atropine, 2mg/kg, i.p., 2-PAM, 25mg/kg, i.m. and diazepam, 5mg/kg, i.p.) promptly stopped SE and reduced acute mortality to 12% and chronic mortality to 18%. This model is ideally suited to test effective countermeasures against lethal POX exposure. Animals that survived the POX SE manifested prolonged elevations in hippocampal [Ca(2+)]i (Ca(2+) plateau) and significant multifocal neuronal injury. POX SE induced Ca(2+) plateau had its origin in Ca(2+) release from intracellular Ca(2+) stores since inhibition of ryanodine/IP3 receptor lowered elevated Ca(2+) levels post SE. POX SE induced neuronal injury and alterations in Ca(2+) dynamics may underlie some of the long term morbidity associated with OP toxicity.

Indexed as

AnimalsAnticonvulsantsAtropineBrainCalciumDiazepamDisease Models, AnimalElectroencephalographyHippocampusMaleNeuronsOrganophosphate PoisoningParaoxonPralidoxime CompoundsRatsRats, Sprague-DawleyAnticonvulsantsAtropineCalciumDiazepamParaoxonpralidoximePralidoxime CompoundsCa(2+) dynamicsParaoxonSprague–Dawley ratsStatus epilepticusSurvival model

Identifiers

PMID24785379
PMCPMC4176600
OpenAlexW2041546653

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.