Alterations in cerebral and cardiac mitochondrial function in a porcine model of acute carbon monoxide poisoning

The 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. Two group large animal model of CO poisoning. Laboratory. Ten swine were divided into two groups: Control (n = 4) and CO (n = 6). Ad...

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Published inClinical toxicology (Philadelphia, Pa.) Vol. 59; no. 9; pp. 801 - 809
Main Authors Jang, David H., Piel, Sarah, Greenwood, John C., Kelly, Matthew, Mazandi, Vanessa M., Ranganathan, Abhay, Lin, Yuxi, Starr, Jonathan, Hallowell, Thomas, Shofer, Frances S., Baker, Wesley B., Lafontant, Alec, Andersen, Kristen, Ehinger, Johannes K., Kilbaugh, Todd J.
Format Journal Article
LanguageEnglish
Published England Taylor & Francis 02.09.2021
Subjects
Animals
Basic Medicine
Carbon Monoxide Poisoning - physiopathology
Cardiology and Cardiovascular Disease
Cell Respiration - physiology
Cerebrovascular Circulation - physiology
Cerebrum - blood supply
Cerebrum - metabolism
Cerebrum - physiopathology
Clinical Medicine
CNS/psychological
complications of poisoning
Disease Models, Animal
Fysiologi och anatomi
Heart - physiopathology
Heart Function Tests
Humans
Kardiologi och kardiovaskulära sjukdomar
Klinisk medicin
Medical and Health Sciences
Medicin och hälsovetenskap
Medicinska och farmaceutiska grundvetenskaper
metabolic
Mitochondria - metabolism
organ/tissue specific
other
Physiology and Anatomy
Swine
organ/tissue specific
other
complications of poisoning
CNS/psychological
metabolic
Online AccessGet full text
ISSN1556-3650
1556-9519
1556-9519
DOI10.1080/15563650.2020.1870691

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Abstract The 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. Two group large animal model of CO poisoning. Laboratory. Ten swine were divided into two groups: Control (n = 4) and CO (n = 6). Administration 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. 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. Animals 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. Low-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.
AbstractList The 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.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.Two group large animal model of CO poisoning.DESIGNTwo group large animal model of CO poisoning.Laboratory.SETTINGLaboratory.Ten swine were divided into two groups: Control (n = 4) and CO (n = 6).SUBJECTSTen swine were divided into two groups: Control (n = 4) and CO (n = 6).Administration 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.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.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.MEASUREMENTSNon-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.Animals 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.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.Low-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.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.
The 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. Two group large animal model of CO poisoning. Laboratory. Ten swine were divided into two groups: Control (n = 4) and CO (n = 6). Administration 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. 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. Animals 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. Low-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.
The 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. Two group large animal model of CO poisoning. Laboratory. Ten swine were divided into two groups: Control (  = 4) and CO (  = 6). Administration 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. 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. Animals 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. Low-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.
Objectives: The 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. Design: Two group large animal model of CO poisoning. Setting: Laboratory. Subjects: Ten swine were divided into two groups: Control (n = 4) and CO (n = 6). Interventions: Administration 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 results: Animals 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. Conclusions: Low-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.
Author Kilbaugh, Todd J.
Shofer, Frances S.
Greenwood, John C.
Kelly, Matthew
Lafontant, Alec
Lin, Yuxi
Jang, David H.
Piel, Sarah
Ranganathan, Abhay
Andersen, Kristen
Ehinger, Johannes K.
Baker, Wesley B.
Starr, Jonathan
Mazandi, Vanessa M.
Hallowell, Thomas
AuthorAffiliation b Resuscitation Science Center, Philadelphia, PA, USA
g Department of Otorhinolaryngology, Head and Neck Surgery, Skåne University Hospital, Lund University, Malmo, Sweden
d Department of Emergency Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
a Department of Emergency Medicine, Division of Medical Toxicology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
e Department of Pediatric Neurology, The Children’s Hospital of Philadelphia (CHOP), Philadelphia, PA, USA
f Mitochondrial Medicine, Department of Clinical Sciences Lund, Lund University, Lund, Sweden
c Department of Anesthesiology and Critical Care Medicine, Department of Emergency Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
AuthorAffiliation_xml – name: e Department of Pediatric Neurology, The Children’s Hospital of Philadelphia (CHOP), Philadelphia, PA, USA
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Snippet The purpose of this study is the development of a porcine model of carbon monoxide (CO) poisoning to investigate alterations in brain and heart mitochondrial...
Objectives: The purpose of this study is the development of a porcine model of carbon monoxide (CO) poisoning to investigate alterations in brain and heart...
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SubjectTerms Animals
Basic Medicine
Carbon Monoxide Poisoning - physiopathology
Cardiology and Cardiovascular Disease
Cell Respiration - physiology
Cerebrovascular Circulation - physiology
Cerebrum - blood supply
Cerebrum - metabolism
Cerebrum - physiopathology
Clinical Medicine
CNS/psychological
complications of poisoning
Disease Models, Animal
Fysiologi och anatomi
Heart - physiopathology
Heart Function Tests
Humans
Kardiologi och kardiovaskulära sjukdomar
Klinisk medicin
Medical and Health Sciences
Medicin och hälsovetenskap
Medicinska och farmaceutiska grundvetenskaper
metabolic
Mitochondria - metabolism
organ/tissue specific
other
Physiology and Anatomy
Swine
Title Alterations in cerebral and cardiac mitochondrial function in a porcine model of acute carbon monoxide poisoning
URI https://www.tandfonline.com/doi/abs/10.1080/15563650.2020.1870691
https://www.ncbi.nlm.nih.gov/pubmed/33529085
https://www.proquest.com/docview/2486147849
https://pubmed.ncbi.nlm.nih.gov/PMC8326298
https://www.ncbi.nlm.nih.gov/pmc/articles/8326298
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