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  1. Article: The Cardiopulmonary Effects of Sodium Fluoroacetate (1080) in Sprague-Dawley Rats.

    McCranor, Bryan J / Young, Talearia D / Tressler, Justin / Jennings, Laura / Irwin, James / Alli, Nazira A / Abilez, Marilynda K / Stone, Samuel / Racine, Michelle / Devorak, Jennifer L / Sciuto, Alfred M / Wong, Benjamin

    Cogent biology

    2019  Volume 5, Issue 1

    Abstract: Sodium fluoroacetate (1080) is a highly toxic metabolic poison that has the potential because of its lack of defined color, odor, and taste and its high water solubility to be intentionally or unintentionally ingested through food adulteration. Although ... ...

    Abstract Sodium fluoroacetate (1080) is a highly toxic metabolic poison that has the potential because of its lack of defined color, odor, and taste and its high water solubility to be intentionally or unintentionally ingested through food adulteration. Although the mechanism of action for 1080 has been known since the 1950's, no known antidote exists. In an effort to better understand the cardiopulmonary impacts of 1080, we utilized whole-body plethysmography and telemeterized Sprague-Dawley rats which allowed for the real-time measurement of respiratory and cardiac parameters following exposure using a non-invasive assisted-drinking method. Overall, the animals showed marked depression of respiratory parameters over the course of 24 hours post-exposure and the development of hemorrhage in the lung tissue. Tidal volume was reduced by 30% in males and 60% in females at 24 hours post-exposure, and respiratory frequency was significantly depressed as well. In telemeterized female rats, we observed severe cardiac abnormalities, highlighted by a 50% reduction in heart rate, 75% reduction in systolic blood pressure, and a 3.5-fold lengthening of the QRS interval over the course of 24 hours. We also observed a reduction in core body temperature of nearly 15°C. Our study was able to describe the severe and pronounced effects of sodium fluoroacetate poisoning on cardiopulmonary function, the results of which indicate that both tissue specific and systemic deficits contribute to the toxicological progression of 1080 intoxication and will need to be accounted for when developing any potential countermeasure for 1080 poisoning.
    Language English
    Publishing date 2019-01-31
    Publishing country England
    Document type Journal Article
    ZDB-ID 2837326-1
    ISSN 2331-2025
    ISSN 2331-2025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: The cardiopulmonary effects of sodium fluoroacetate (1080) in Sprague-Dawley rats

    McCranor, Bryan J / Young, Talearia D / Tressler, Justin / Jennings, Laura / Irwin, James / Alli, Nazira A / Abilez, Marilynda K / Stone, Samuel / Racine, Michelle / Devorak, Jennifer L / Sciuto, Alfred M / Wong, Benjamin / Zang, Tianzhu

    Cogent biology. 2019 Jan. 01, v. 5, no. 1

    2019  

    Abstract: Sodium fluoroacetate (1080) is a highly toxic metabolic poison that has the potential because of its lack of defined color, odor, and taste and its high water solubility to be intentionally or unintentionally ingested through food adulteration. Although ... ...

    Abstract Sodium fluoroacetate (1080) is a highly toxic metabolic poison that has the potential because of its lack of defined color, odor, and taste and its high water solubility to be intentionally or unintentionally ingested through food adulteration. Although the mechanism of action for 1080 has been known since the 1950s, no known antidote exists. In an effort to better understand the cardiopulmonary impacts of 1080, we utilized whole-body plethysmography and telemeterized Sprague-Dawley rats which allowed for the real-time measurement of respiratory and cardiac parameters following exposure using a non-invasive assisted-drinking method. Overall, the animals showed marked depression of respiratory parameters over the course of 24 h post-exposure and the development of hemorrhage in the lung tissue. Tidal volume was reduced by 30% in males and 60% in females at 24 h post-exposure, and respiratory frequency was significantly depressed as well. In telemeterized female rats, we observed severe cardiac abnormalities, highlighted by a 50% reduction in heart rate, 75% reduction in systolic blood pressure, and a 3.5-fold lengthening of the QRS interval over the course of 24 h. We also observed a reduction in core body temperature of nearly 15°C. Our study was able to describe the severe and pronounced effects of sodium fluoroacetate poisoning on cardiopulmonary function, the results of which indicate that both tissue specific and systemic deficits contribute to the toxicological progression of 1080 intoxication and will need to be accounted for when developing any potential countermeasure for 1080 poisoning.
    Keywords adulterated foods ; antidotes ; body temperature ; color ; females ; heart rate ; hemorrhage ; lungs ; mechanism of action ; odors ; plethysmography ; poisoning ; respiratory rate ; sodium fluoroacetate ; systolic blood pressure ; taste ; tidal volume ; toxicity ; toxicology ; water solubility
    Language English
    Dates of publication 2019-0101
    Publishing place Cogent
    Document type Article
    Note NAL-AP-2-clean
    ZDB-ID 2837326-1
    ISSN 2331-2025
    ISSN 2331-2025
    DOI 10.1080/23312025.2019.1568669
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Vapor inhalation exposure to soman in conscious untreated rats: preliminary assessment of neurotoxicity.

    Perkins, Michael W / Wong, Benjamin / Rodriguez, Ashley / Devorak, Jennifer L / Dao, Thuy T / Leuschner, Jessica A / Kan, Robert K / Sciuto, Alfred M

    Inhalation toxicology

    2016  Volume 28, Issue 1, Page(s) 14–21

    Abstract: Neurological toxicity and brain injury following vapor inhalation exposure to the chemical warfare nerve agent (CWNA) soman (GD) were examined in untreated non-anesthetized rats. In this study, male Sprague-Dawley rats (300-350 g) were exposed to 600 mg × ...

    Abstract Neurological toxicity and brain injury following vapor inhalation exposure to the chemical warfare nerve agent (CWNA) soman (GD) were examined in untreated non-anesthetized rats. In this study, male Sprague-Dawley rats (300-350 g) were exposed to 600 mg × min/m(3) of soman or vehicle in a customized head-out inhalation system for 7 min. Convulsant animals were observed for clinical signs and various regions of the brain (dorsolateral thalamus, basolateral amygdala, piriform cortex, and lateral cortex) were collected for pathological observations 24 h post-exposure. Signs of CWNA-induced cholinergic crises including salivation, lacrimation, increased urination and defecation, and tremors were observed in all soman-exposed animals. Soman-exposed animals at 24 h post-exposure lost 11% of their body weight in comparison to 2% in vehicle-exposed animals. Whole blood acetylcholinesterase (AChE) activity was significantly inhibited in all soman-exposed groups in comparison to controls. Brain injury was confirmed by the neurological assessment of hematoxylin-eosin (H&E) staining and microscopy in the piriform cortex, dorsolateral thalamus, basolateral amygdala, and lateral cortex. Severe damage including prominent lesions, edematous, congested, and/or hemorrhagic tissues was observed in the piriform cortex, dorsolateral thalamus, and lateral cortex in soman-exposed animals 24 h post-exposure, while only minimal damage was observed in the basolateral amygdala. These results indicate that inhalation exposure to soman vapor causes neurological toxicity and brain injury in untreated unanesthetized rats. This study demonstrates the ability of the described soman vapor inhalation exposure model to cause neurological damage 24 h post-exposure in rats.
    MeSH term(s) Acetylcholinesterase/blood ; Administration, Inhalation ; Animals ; Body Weight/drug effects ; Brain/drug effects ; Brain/pathology ; Chemical Warfare Agents/toxicity ; Male ; Neurotoxicity Syndromes/blood ; Neurotoxicity Syndromes/etiology ; Neurotoxicity Syndromes/pathology ; Rats, Sprague-Dawley ; Soman/toxicity
    Chemical Substances Chemical Warfare Agents ; Soman (96-64-0) ; Acetylcholinesterase (EC 3.1.1.7)
    Language English
    Publishing date 2016
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1038809-6
    ISSN 1091-7691 ; 0895-8378
    ISSN (online) 1091-7691
    ISSN 0895-8378
    DOI 10.3109/08958378.2015.1125973
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2618: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Inhalation toxicity of soman vapor in non-anesthetized rats: A preliminary assessment of inhaled bronchodilator or steroid therapy

    Perkins, Michael W / Wong, Benjamin / Rodriguez, Ashley / Devorak, Jennifer L / Alves, Derron A / Murphy, Gleeson / Sciuto, Alfred M

    Chemico-biological interactions. 2013 Dec. 5, v. 206, no. 3

    2013  

    Abstract: Respiratory toxicity, injury and treatment following vapor inhalational exposure to the chemical warfare nerve agent (CWNA) soman (GD) were examined in non-anesthetized rats. This study exposed male Sprague–Dawley rats (250–300g) to 520, 560, 600, 825 or ...

    Abstract Respiratory toxicity, injury and treatment following vapor inhalational exposure to the chemical warfare nerve agent (CWNA) soman (GD) were examined in non-anesthetized rats. This study exposed male Sprague–Dawley rats (250–300g) to 520, 560, 600, 825 or 1410mg×min/m³ of soman in a customized head-out inhalation system. Signs of CWNA-induced cholinergic crises were observed in all soman-exposed animals. The LCt50 of vaporized soman as determined by probit analysis was 593.1mg×min/m³. All animals exposed to 825 and 1410mg×min/m³ developed severe convulsions and died within 4–8min post-exposure. Edema measured by wet/dry weight ratio of the left lung lobe increased in a dose-dependent manner in all soman-exposed animals. Bronchoalveolar lavage (BAL) fluid and blood acetylcholinesterase (AChE) activities were inhibited dose-dependently in soman-exposed groups at 24h. A significant increase in total BAL protein was observed in soman-exposed animals at all doses. AChE activity was inhibited in lung and whole brain tissues in all soman-exposed animals. Histopathological analysis of the lungs of animals exposed to 600mg×min/m³ of soman revealed prominent morphological changes including alveolar histiocytosis, hemorrhage and inflammation consisting of neutrophilic exudate. Exposure of animals to 600mg×min/m³ of soman followed by treatment with two actuations for 10s of Combivent (21μg of ipratropium bromide and 120μg of albuterol sulfate) and Symbicort (80μg budesonide and 4.5μg formoterol) by inhalation into a modified metered dose inhaler (MDI) 10min post-exposure resulted in increased minute volume, but did not decrease mortality. These results indicate that inhalation exposure to soman vapor causes acute respiratory toxicity and injury in untreated, un-anesthetized rats and that inhalation treatment with Combivent or Symbicort did improve the respiratory outcomes, but did not influence lethality.
    Keywords acetylcholinesterase ; blood ; brain ; breathing ; edema ; hemorrhage ; histiocytosis ; histopathology ; inflammation ; inhalation exposure ; lungs ; mortality ; nerve tissue ; probit analysis ; rats ; seizures ; therapeutics ; toxicity ; vapors
    Language English
    Dates of publication 2013-1205
    Size p. 452-461.
    Publishing place Elsevier Ireland Ltd
    Document type Article
    ZDB-ID 218799-1
    ISSN 1872-7786 ; 0009-2797
    ISSN (online) 1872-7786
    ISSN 0009-2797
    DOI 10.1016/j.cbi.2013.07.009
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 75/703: Show issues

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  5. Article ; Online: Inhalation toxicity of soman vapor in non-anesthetized rats: a preliminary assessment of inhaled bronchodilator or steroid therapy.

    Perkins, Michael W / Wong, Benjamin / Rodriguez, Ashley / Devorak, Jennifer L / Alves, Derron A / Murphy, Gleeson / Sciuto, Alfred M

    Chemico-biological interactions

    2013  Volume 206, Issue 3, Page(s) 452–461

    Abstract: Respiratory toxicity, injury and treatment following vapor inhalational exposure to the chemical warfare nerve agent (CWNA) soman (GD) were examined in non-anesthetized rats. This study exposed male Sprague-Dawley rats (250-300g) to 520, 560, 600, 825 or ...

    Abstract Respiratory toxicity, injury and treatment following vapor inhalational exposure to the chemical warfare nerve agent (CWNA) soman (GD) were examined in non-anesthetized rats. This study exposed male Sprague-Dawley rats (250-300g) to 520, 560, 600, 825 or 1410mg×min/m(3) of soman in a customized head-out inhalation system. Signs of CWNA-induced cholinergic crises were observed in all soman-exposed animals. The LCt50 of vaporized soman as determined by probit analysis was 593.1mg×min/m(3). All animals exposed to 825 and 1410mg×min/m(3) developed severe convulsions and died within 4-8min post-exposure. Edema measured by wet/dry weight ratio of the left lung lobe increased in a dose-dependent manner in all soman-exposed animals. Bronchoalveolar lavage (BAL) fluid and blood acetylcholinesterase (AChE) activities were inhibited dose-dependently in soman-exposed groups at 24h. A significant increase in total BAL protein was observed in soman-exposed animals at all doses. AChE activity was inhibited in lung and whole brain tissues in all soman-exposed animals. Histopathological analysis of the lungs of animals exposed to 600mg×min/m(3) of soman revealed prominent morphological changes including alveolar histiocytosis, hemorrhage and inflammation consisting of neutrophilic exudate. Exposure of animals to 600mg×min/m(3) of soman followed by treatment with two actuations for 10s of Combivent (21μg of ipratropium bromide and 120μg of albuterol sulfate) and Symbicort (80μg budesonide and 4.5μg formoterol) by inhalation into a modified metered dose inhaler (MDI) 10min post-exposure resulted in increased minute volume, but did not decrease mortality. These results indicate that inhalation exposure to soman vapor causes acute respiratory toxicity and injury in untreated, un-anesthetized rats and that inhalation treatment with Combivent or Symbicort did improve the respiratory outcomes, but did not influence lethality.
    MeSH term(s) Acetylcholinesterase/blood ; Acetylcholinesterase/metabolism ; Acute Lung Injury/drug therapy ; Acute Lung Injury/pathology ; Acute Lung Injury/physiopathology ; Administration, Inhalation ; Adrenal Cortex Hormones/administration & dosage ; Albuterol/administration & dosage ; Albuterol, Ipratropium Drug Combination ; Animals ; Brain/drug effects ; Brain/enzymology ; Bronchodilator Agents/administration & dosage ; Budesonide/administration & dosage ; Budesonide, Formoterol Fumarate Drug Combination ; Chemical Warfare Agents/toxicity ; Disease Models, Animal ; Drug Combinations ; Ethanolamines/administration & dosage ; Inhalation Exposure ; Ipratropium/administration & dosage ; Lung/drug effects ; Lung/enzymology ; Lung/pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Soman/administration & dosage ; Soman/toxicity
    Chemical Substances Adrenal Cortex Hormones ; Albuterol, Ipratropium Drug Combination ; Bronchodilator Agents ; Budesonide, Formoterol Fumarate Drug Combination ; Chemical Warfare Agents ; Drug Combinations ; Ethanolamines ; Budesonide (51333-22-3) ; Soman (96-64-0) ; Acetylcholinesterase (EC 3.1.1.7) ; Ipratropium (GR88G0I6UL) ; Albuterol (QF8SVZ843E)
    Language English
    Publishing date 2013-12-05
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218799-1
    ISSN 1872-7786 ; 0009-2797
    ISSN (online) 1872-7786
    ISSN 0009-2797
    DOI 10.1016/j.cbi.2013.07.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 686: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article: Inhalation toxicity of soman vapor in non-anesthetized rats: A preliminary assessment of inhaled bronchodilator or steroid therapy

    Perkins, Michael W. / Wong, Benjamin / Rodriguez, Ashley / Devorak, Jennifer L. / Alves, Derron A. / Murphy, Gleeson / Sciuto, Alfred M.

    Chemico-biological interactions

    Volume v. 206,, Issue no. 3

    Abstract: Respiratory toxicity, injury and treatment following vapor inhalational exposure to the chemical warfare nerve agent (CWNA) soman (GD) were examined in non-anesthetized rats. This study exposed male Sprague–Dawley rats (250–300g) to 520, 560, 600, 825 or ...

    Abstract Respiratory toxicity, injury and treatment following vapor inhalational exposure to the chemical warfare nerve agent (CWNA) soman (GD) were examined in non-anesthetized rats. This study exposed male Sprague–Dawley rats (250–300g) to 520, 560, 600, 825 or 1410mg×min/m³ of soman in a customized head-out inhalation system. Signs of CWNA-induced cholinergic crises were observed in all soman-exposed animals. The LCt50 of vaporized soman as determined by probit analysis was 593.1mg×min/m³. All animals exposed to 825 and 1410mg×min/m³ developed severe convulsions and died within 4–8min post-exposure. Edema measured by wet/dry weight ratio of the left lung lobe increased in a dose-dependent manner in all soman-exposed animals. Bronchoalveolar lavage (BAL) fluid and blood acetylcholinesterase (AChE) activities were inhibited dose-dependently in soman-exposed groups at 24h. A significant increase in total BAL protein was observed in soman-exposed animals at all doses. AChE activity was inhibited in lung and whole brain tissues in all soman-exposed animals. Histopathological analysis of the lungs of animals exposed to 600mg×min/m³ of soman revealed prominent morphological changes including alveolar histiocytosis, hemorrhage and inflammation consisting of neutrophilic exudate. Exposure of animals to 600mg×min/m³ of soman followed by treatment with two actuations for 10s of Combivent (21μg of ipratropium bromide and 120μg of albuterol sulfate) and Symbicort (80μg budesonide and 4.5μg formoterol) by inhalation into a modified metered dose inhaler (MDI) 10min post-exposure resulted in increased minute volume, but did not decrease mortality. These results indicate that inhalation exposure to soman vapor causes acute respiratory toxicity and injury in untreated, un-anesthetized rats and that inhalation treatment with Combivent or Symbicort did improve the respiratory outcomes, but did not influence lethality.
    Keywords therapeutics ; inflammation ; histiocytosis ; inhalation exposure ; lungs ; breathing ; histopathology ; probit analysis ; blood ; nerve tissue ; toxicity ; vapors ; seizures ; edema ; mortality ; acetylcholinesterase ; rats ; brain ; hemorrhage
    Language English
    Document type Article
    ISSN 0009-2797
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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