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Free radicals and myocardial reperfusion injury
Abstract
Ischaemic myocardial tissue will, inevitably, necrose if blood flow is not restored. Whilst reperfusion is always beneficial in terms of potential recovery of heart muscle, reperfusion in itself is believed to bring about cellular injury. While the causes of this 'reperfusion injury' are apparently multifactorial, there is now an increasing body of evidence to suggest that oxygen free radicals play a major role in the pathogenesis of reperfusion injury. The initial evidence for this hypothesis was indirect, based on the ability of free radical scavengers to limit myocardial injury in animal models. More recent work has utilised the highly specific technique of electron spin resonance (ESR) spectroscopy and ESR spin trapping to detect the free radical species. The evidence for free radical production on myocardial reperfusion will be presented along with details of human studies. The potential for a therapeutic intervention will also be briefly discussed.
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“Endogenous NO• modulates respiration by its effect to compete reversibly for the O2 binding site on cytochrome c oxidase (complex IV) (45, 58, 119).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [119]
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Cited by
Stowe, D. F., & Camara, A. K. S. (2009) · Antioxidants & Redox Signaling · doi:10.1089/ars.2008.2331 · Cited by 471
“Tissue damage during hypoxia and reperfusion after ischemia has long been known to be associated with increased levels of various ROS (6, 15, 19, 123, 170, 290, 309, 318).”
BackgroundOxidative stress and cardiac disease
Lefer, D. J., & Granger, D. N. (2000) · The American Journal of Medicine · doi:10.1016/s0002-9343(00)00467-8 · Cited by 449
Update on the Biological Characteristics of the Antioxidant Micronutrients
ROCK, C. L., JACOB, R. A., & BOWEN, P. E. (1996) · Journal of the American Dietetic Association · doi:10.1016/s0002-8223(96)00190-3 · Cited by 308
Davies, M. J. (2016) · Methods · doi:10.1016/j.ymeth.2016.05.013 · Cited by 272
Detection and characterisation of radicals in biological materials using EPR methodology
Hawkins, C. L., & Davies, M. J. (2013) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2013.03.034 · Cited by 253
Metadata
- Authors
- Flitter, W. D.
- Affiliations
- Brunel University of London (GB)
- Corresponding author
- Flitter, W D
- Venue
- British Medical Bulletin
- Publisher
- Oxford University Press (OUP)
- Published
- 1993
- Volume
- 49
- Issue
- 3
- Pages
- 545-555
- ISSN
- 0007-1420 (ISSN-L)
- 1471-8391
- OpenAlex
- W2336213290
- Cited by
- 69
- References
- 0
- Citations by year
- 2023: 1 · 2021: 1 · 2020: 2 · 2018: 1 · 2017: 1 · 2016: 3 · 2014: 2 · 2013: 3 · 2012: 2
- FWCI
- 1.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- British Medical Bulletin (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- free radicals, myocardial ischemia-reperfusion injury, oxygen free radicals, myocardial ischemia, radical scavengers, electron spin resonance spectroscopy, EPR spin trapping, therapeutic interventions
- MeSH terms
- Animals, Dogs, Free Radicals, Guinea Pigs, Humans, Myocardial Infarction, Myocardium, Oxidation-Reduction, Oxygen, Rabbits, Xanthine Dehydrogenase, Xanthine Oxidase, Myocardial Reperfusion Injury, Reactive Oxygen Species, Thiobarbituric Acid Reactive Substances, Mice
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- The paper
- Flitter, W. D. (1993). Free radicals and myocardial reperfusion injury. British Medical Bulletin. https://doi.org/10.1093/oxfordjournals.bmb.a072629
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.