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The role of lipid peroxidation in pathogenesis of ischemic damage and the antioxidant protection of the heart.

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TLDR
The proposed hypothesis and experimental data underly successful application of synthetic free radical scavengers (antioxidants) for heart protection against experimental myocardial infarction, transitory ischemia, and emotional, painful stress.
Abstract
A working hypothesis on pathogenesis of ischemic heart damage has been proposed. According to this hypothesis, a crucial role in conversion of reversible damage into irreversible damage is played by cardiomyocyte membrane destruction caused by the so-called “lipid triad”. The latter comprises activation of lipid peroxidation, activation of phospholipases, and the degergentlike action of excessive amounts of free fatty acids and lysophospholipids. Marked activation of lipid peroxidation in experimental myocardial infarction, as well as reoxygenation following transitory ischemia, have been demonstrated. The proposed hypothesis and experimental data underly successful application of synthetic free radical scavengers (antioxidants) for heart protection against experimental myocardial infarction, transitory ischemia, and emotional, painful stress.

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Citations
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Journal ArticleDOI

Oxygen-derived free radicals in postischemic tissue injury.

TL;DR: It is now clear that oxygen-derived free radicals play an important part in several models of experimentally induced reperfusion injury, and Dysfunction induced by free radicals may be a major component of ischemic diseases of the heart, bowel, liver, kidney, and brain.
Journal ArticleDOI

Role of oxidative stress in cardiovascular diseases.

TL;DR: The existing evidence support the view that oxidative stress may play a crucial role in cardiac and vascular abnormalities in different types of cardiovascular diseases and that the antioxidant therapy may prove beneficial in combating these problems.
Journal ArticleDOI

Canine myocardial reperfusion injury. Its reduction by the combined administration of superoxide dismutase and catalase.

TL;DR: The results of this investigation demonstrate that the ‘primary’ myqcardial cellular damage due to ischemia is additive to the cardiac cell damage during the phase of reperfusion, and that the“secondary” effects are mediated by toxic metabolites of oxygen.
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Xanthine oxidase as a source of free radical damage in myocardial ischemia.

TL;DR: The infarcts in the allopurinol and superoxide dismutase groups were significantly smaller than those in the control groups, and the xanthine oxidase/xanthine dehydrogenase content of dog myocardium was determined.
References
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BRIEF REVIEWS Lipid-Membrane Interactions and the Pathogenesis of Ischemic Damage in the Myocardium

TL;DR: A large body of evidence now indicates that altered lipid metabolism can alter cardiac function by changing the properties of cardiac cell membranes, and that these functional changes may contribute to the decline in myocardial contractility, the arrhythmias, and the eventual cell death that follow coronary artery occlusion.
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Role of oxygen in the cellular damage induced by re-oxygenation of hypoxic heart.

TL;DR: It is suggested that re-oxygenation is able to induce lipid peroxidative damage in cardiac rat tissue when hypoxic substrate-free perfusions had previously reduced the cellular defensive mechanisms capable of neutralizing the toxic reactions mediated by oxygen metabolites.
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Abrupt reoxygenation of the anoxic potassium-arrested perfused rat heart: a study of myocardial enzyme release.

TL;DR: Reoxygenation of the heart during phase 2 of enzyme release resulted in an immediate and massive increase in the rate of protein and enzyme release from the myocardium.
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Ischemic contracture of the heart: “Stone heart”

TL;DR: Ultimately, cardiopulmonary bypass cannot be discontinued without the patient dying because of the maintained contractile state, so this irreversibly contracted ventricle of myocardial failure is named the “stone heart.”
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