ArticleMolecular and cellular biochemistry2015
Phospholipid alterations in the brain and heart in a rat model of asphyxia-induced cardiac arrest and cardiopulmonary bypass resuscitation.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 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
- Exploring Lysophosphatidylcholine as a Biomarker in Ischemic Stroke: The Plasma-Brain Disjunction.International journal of molecular sciences · 2024Article
- The Role of Phospholipid Alterations in Mitochondrial and Brain Dysfunction after Cardiac Arrest.International journal of molecular sciences · 2024Review
- Article
- 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
- Pharmacological Approach for Neuroprotection After Cardiac Arrest-A Narrative Review of Current Therapies and Future Neuroprotective Cocktail.Frontiers in medicine · 2021Review
- Cannabinoid Receptor Agonist WIN55, 212-2 Adjusts Lipid Metabolism in a Rat Model of Cardiac Arrest.Therapeutic hypothermia and temperature management · 2020Article
- Plasma metabolomics supports the use of long-duration cardiac arrest rodent model to study human disease by demonstrating similar metabolic alterations.Scientific reports · 2020Article
- Plasma Metabolomic Profiles Differentiate Patients With Dilated Cardiomyopathy and Ischemic Cardiomyopathy.Frontiers in cardiovascular medicine · 2020Article
- Relative Ratios Enhance the Diagnostic Power of Phospholipids in Distinguishing Benign and Cancerous Ovarian Masses.Cancers · 2019Article
- Tissue-Specific Metabolic Profiles After Prolonged Cardiac Arrest Reveal Brain Metabolome Dysfunction Predominantly After Resuscitation.Journal of the American Heart Association · 2019Article
- l-α-Lysophosphatidylinositol (LPI) aggravates myocardial ischemia/reperfusion injury via a GPR55/ROCK-dependent pathway.Pharmacology research & perspectives · 2019Article
- Challenges and Inconsistencies in Using Lysophosphatidic Acid as a Biomarker for Ovarian Cancer.Cancers · 2019Article
- Increased Survival Time With SS-31 After Prolonged Cardiac Arrest in Rats.Heart, lung & circulation · 2019Article
- Recent advances in personalizing cardiac arrest resuscitation.F1000Research · 2019Review
- Integrated UPLC-Q/TOF-MS Technique and MALDI-MS to Study of the Efficacy of YiXinshu Capsules Against Heart Failure in a Rat Model.Frontiers in pharmacology · 2019Article
- Comparing phospholipid profiles of mitochondria and whole tissue: Higher PUFA content in mitochondria is driven by increased phosphatidylcholine unsaturation.Journal of chromatography. B, Analytical technologies in the biomedical and life sciences · 2018Article
- Comprehensive analysis of phospholipids in the brain, heart, kidney, and liver: brain phospholipids are least enriched with polyunsaturated fatty acids.Molecular and cellular biochemistry · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac arrest (CA) induces whole-body ischemia, causing damage to multiple organs. Ischemic damage to the brain is mainly responsible for patient mortality. However, the molecular mechanism responsible for brain damage is not understood. Prior studies have provided evidence that degradation of membrane phospholipids plays key roles in ischemia/reperfusion injury. The aim of this study is to correlate organ damage to phospholipid alterations following 30 min asphyxia-induced CA or CA followed by cardiopulmonary bypass (CPB) resuscitation using a rat model. Following 30 min CA and CPB resuscitation, rats showed no brain function, moderately compromised heart function, and died within a few hours; typical outcomes of severe CA. However, we did not find any significant change in the content or composition of phospholipids in either tissue following 30 min CA or CA followed by CPB resuscitation. We found a substantial increase in lysophosphatidylinositol in both tissues, and a small increase in lysophosphatidylethanolamine and lysophosphatidylcholine only in brain tissue following CA. CPB resuscitation significantly decreased lysophosphatidylinositol but did not alter the other lyso species. These results indicate that a decrease in phospholipids is not a cause of brain damage in CA or a characteristic of brain ischemia. However, a significant increase in lysophosphatidylcholine and lysophosphatidylethanolamine found only in the brain with more damage suggests that impaired phospholipid metabolism may be correlated with the severity of ischemia in CA. In addition, the unique response of lysophosphatidylinositol suggests that phosphatidylinositol metabolism is highly sensitive to cellular conditions altered by ischemia and resuscitation.
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