ArticleClinical toxicology (Philadelphia, Pa.)2021
Alterations in cerebral and cardiac mitochondrial function in a porcine model of acute carbon monoxide poisoning.
Article in Clinical toxicology (Philadelphia, Pa.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Mitochondrial dysfunction, cerebral metabolic crisis, and exploratory bioenergetic biomarkers in a translational swine model of acute carbon monoxide poisoning.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Dose-dependent cerebral metabolic impairment in a swine model of carbon monoxide poisoning.Neurotoxicology · 2026Article
- Attenuation of mitochondrial dysfunction in a ventricular fibrillation swine model of cardiac arrest treated with carbon monoxide.Resuscitation · 2025Article
- Blood Cells as a Cellular Biomarker for Mitochondrial Function in a Experimental Model of Acute Carbon Monoxide Poisoning with Treatment.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2025Article
- Effect of dimethyl fumarate on mitochondrial metabolism in a pediatric porcine model of asphyxia-induced in-hospital cardiac arrest.Scientific reports · 2024Article
- Investigation of Cerebral Mitochondrial Injury in a Porcine Survivor Model of Carbon Monoxide Poisoning.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2024Article
- Carbon monoxide as a cellular protective agent in a swine model of cardiac arrest protocol.PloS one · 2024Article
- Cell-Free DNA as a Biomarker in a Rodent Model of Chlorpyrifos Poisoning Causing Mitochondrial Dysfunction.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2023Article
- Succinate prodrugs as treatment for acute metabolic crisis during fluoroacetate intoxication in the rat.Molecular and cellular biochemistry · 2023Article
- Alteration in Cerebral Metabolism in a Rodent Model of Acute Sub-lethal Cyanide Poisoning.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2023Article
- Succinate prodrugs in combination with atropine and pralidoxime protect cerebral mitochondrial function in a rodent model of acute organophosphate poisoning.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
objectivesThe purpose of this study is the development of a porcine model of carbon monoxide (CO) poisoning to investigate alterations in brain and heart mitochondrial function.
designTwo group large animal model of CO poisoning.
settingLaboratory. SUBJECTS: Ten swine were divided into two groups: Control (
interventionsAdministration of a low dose of CO at 200 ppm to the CO group over 90 min followed by 30 min of re-oxygenation at room air. The Control group received room air for 120 min. MEASUREMENTS: Non-invasive optical monitoring was used to measure cerebral blood flow and oxygenation. Cerebral microdialysis was performed to obtain semi real time measurements of cerebral metabolic status. At the end of the exposure, both fresh brain (cortical and hippocampal tissue) and heart (apical tissue) were immediately harvested to measure mitochondrial respiration and reactive oxygen species (ROS) generation and blood was collected to assess plasma cytokine concentrations. MAIN
resultsAnimals in the CO group showed significantly decreased Complex IV-linked mitochondrial respiration in hippocampal and apical heart tissue but not cortical tissue. There also was a significant increase in mitochondrial ROS generation across all measured tissue types. The CO group showed a significantly higher cerebral lactate-to-pyruvate ratio. Both IL-8 and TNFα were significantly increased in the CO group compared with the Control group obtained from plasma. While not significant there was a trend to an increase in optically measured cerebral blood flow and hemoglobin concentration in the CO group.
conclusionsLow-dose CO poisoning is associated with early mitochondrial disruption prior to an observable phenotype highlighting the important role of mitochondrial function in the pathology of CO poisoning. This may represent an important intervenable pathway for therapy and intervention.
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