ArticlePloS one2014
Examination of physiological function and biochemical disorders in a rat model of prolonged asphyxia-induced cardiac arrest followed by cardio pulmonary bypass resuscitation.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Species-selective plasma metabolism drives lysophosphatidylcholine depletion after cardiac arrest.The Journal of biological chemistry · 2026Article
- Improved survival and neurological outcomes with lysophosphatidylcholine supplementation in severe cardiac arrest model.Frontiers in pharmacology · 2025Article
- Therapeutic Administration of Oxcarbazepine Saves Cerebellar Purkinje Cells from Ischemia and Reperfusion Injury Induced by Cardiac Arrest through Attenuation of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Article
- Review
- Hydrogen gas with extracorporeal cardiopulmonary resuscitation improves survival after prolonged cardiac arrest in rats.Journal of translational medicine · 2021Article
- Increased plasma disequilibrium between pro- and anti-oxidants during the early phase resuscitation after cardiac arrest is associated with increased levels of oxidative stress end-products.Molecular medicine (Cambridge, Mass.) · 2021Article
- Plasma metabolomics supports the use of long-duration cardiac arrest rodent model to study human disease by demonstrating similar metabolic alterations.Scientific reports · 2020Article
- Stearic acid methyl ester affords neuroprotection and improves functional outcomes after cardiac arrest.Prostaglandins, leukotrienes, and essential fatty acids · 2020Article
- The JAK2/STAT3 pathway is involved in dexmedetomidine-induced myocardial protection in rats undergoing cardiopulmonary bypass.Annals of translational medicine · 2020Article
- Tissue-Specific Metabolic Profiles After Prolonged Cardiac Arrest Reveal Brain Metabolome Dysfunction Predominantly After Resuscitation.Journal of the American Heart Association · 2019Article
- The role of decreased cardiolipin and impaired electron transport chain in brain damage due to cardiac arrest.Neurochemistry international · 2018Article
- Metabolomics profiling reveals different patterns in an animal model of asphyxial and dysrhythmic cardiac arrest.Scientific reports · 2017Article
- Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model.BMC cardiovascular disorders · 2017Article
- Dexmedetomidine reduces the neuronal apoptosis related to cardiopulmonary bypass by inhibiting activation of the JAK2-STAT3 pathway.Drug design, development and therapy · 2017Article
- DHA-supplemented diet increases the survival of rats following asphyxia-induced cardiac arrest and cardiopulmonary bypass resuscitation.Scientific reports · 2016Article
- The Responses of Tissues from the Brain, Heart, Kidney, and Liver to Resuscitation following Prolonged Cardiac Arrest by Examining Mitochondrial Respiration in Rats.Oxidative medicine and cellular longevity · 2016Article
- Phospholipid alterations in the brain and heart in a rat model of asphyxia-induced cardiac arrest and cardiopulmonary bypass resuscitation.Molecular and cellular biochemistry · 2015Article
- Cardiac arrest: resuscitation and reperfusion.Circulation research · 2015Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCardiac arrest induces whole body ischemia, which causes damage to multiple organs particularly the heart and the brain. There is clinical and preclinical evidence that neurological injury is responsible for high mortality and morbidity of patients even after successful cardiopulmonary resuscitation. A better understanding of the metabolic alterations in the brain during ischemia will enable the development of better targeted resuscitation protocols that repair the ischemic damage and minimize the additional damage caused by reperfusion.
methodA validated whole body model of rodent arrest followed by resuscitation was utilized; animals were randomized into three groups: control, 30 minute asphyxial arrest, or 30 minutes asphyxial arrest followed by 60 min cardiopulmonary bypass (CPB) resuscitation. Blood gases and hemodynamics were monitored during the procedures. An untargeted metabolic survey of heart and brain tissues following cardiac arrest and after CPB resuscitation was conducted to better define the alterations associated with each condition.
resultsAfter 30 min cardiac arrest and 60 min CPB, the rats exhibited no observable brain function and weakened heart function in a physiological assessment. Heart and brain tissues harvested following 30 min ischemia had significant changes in the concentration of metabolites in lipid and carbohydrate metabolism. In addition, the brain had increased lysophospholipid content. CPB resuscitation significantly normalized metabolite concentrations in the heart tissue, but not in the brain tissue.
conclusionThe observation that metabolic alterations are seen primarily during cardiac arrest suggests that the events of ischemia are the major cause of neurological damage in our rat model of asphyxia-CPB resuscitation. Impaired glycolysis and increased lysophospholipids observed only in the brain suggest that altered energy metabolism and phospholipid degradation may be a central mechanism in unresuscitatable brain damage.
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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.