Xanthine oxidase as a source of free radical damage in myocardial ischemia
Abstract
Experiments were performed to determine if xanthine oxidase is a source of free radicals during myocardial ischemia. Open chest dogs were subjected to 1 h of total occlusion of the left anterior descending coronary artery followed by 4 h of reperfusion. Directly after coronary artery occlusion, Ce141 microspheres were injected into the left atrium to mark the ischemic bed. At the end of reperfusion, the hearts were removed and sectioned. Autoradiography determined the ischemic myocardium at risk, and the necrotic zone was determined by triphenyl-tetrazolium staining. Animals were divided into three groups: control, allopurinol (24-h oral pretreatment 400 mg, then 50 mg/kg IV bolus on occlusion); and superoxide dismutase starting with occlusion (15 000 U/kg). The size of the infarct as a percentage of the tissue at risk was: 23.1 +/- 4.1 for the control; 8.7 +/- 1.2 for the allopurinol group; and 5.4 +/- 1.2 for the superoxide dismutase group. The infarcts in the allopurinol and superoxide dismutase groups were significantly smaller than those in the control groups. In a second series of experiments we determined the xanthine oxidase/xanthine dehydrogenase content of dog myocardium. The left anterior descending branch was ligated for 30 min and then biopsies were removed from both the normal and the ischemic regions. Total enzyme content did not differ between the two regions averaging 0.259 U/g protein for the ischemic tissue and 0.225 U/g protein for the normal region. Only 9.8% of the enzyme was in the oxidase form in the normal region while 32.8% was in the oxidase form in the ischemic zone.(ABSTRACT TRUNCATED AT 250 WORDS)
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Extensive evidence supports a role of XO in the development of cardiovascular disease.
“Extensive evidence supports a role of XO in the development of cardiovascular disease (137, 148, 157, 282, 430, 466, 561, 633).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [157]
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- Authors
- CHAMBERS, D., PARKS, D., PATTERSON, G., ROY, R., MCCORD, J., YOSHIDA, S., PARMLEY, L., & DOWNEY, J.
- Affiliations
- University of South Alabama (US)
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 1985-02
- Volume
- 17
- Issue
- 2
- Pages
- 145-152
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W2034683799
- Cited by
- 672
- References
- 52
- Citations by year
- 2025: 2 · 2024: 5 · 2023: 7 · 2022: 5 · 2021: 9 · 2020: 2 · 2019: 10 · 2018: 3 · 2017: 9 · 2015: 7 · 2014: 5 · 2013: 12 · 2012: 8
- FWCI
- 51.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Molecular and Cellular Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
- Keywords
- xanthine oxidase, myocardial ischemia, ischemia-reperfusion injury, free radicals, superoxide, allopurinol, superoxide dismutase, myocardial infarct size, xanthine dehydrogenase, coronary artery occlusion
- MeSH terms
- Allopurinol, Animals, Coronary Circulation, Coronary Disease, Dogs, Female, Free Radicals, Male, Myocardium, Necrosis, Superoxide Dismutase, Xanthine Oxidase
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