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Titlebook: Oxygen Radicals in the Pathophysiology of Heart Disease; Pawan K. Singal Book 1988 Kluwer Academic Publishers 1988 cardiovascular.cardiova

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The Role of Oxygen Free Radicals during the Course of Myocardial Ischemia/Reperfusion Injury: An Anakdown of ATP to hypoxanthine and xanthine, an increase in reducing equivalents and activation of the cyclooxygenase system. All of these reactions favor the univalent reduction of molecular oxygen to free oxygen radicals and their metabolites (superoxide anion, ·O. ., hydrogen peroxide, H.O., and t
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Alterations of Glutathione Status during Myocardial Ischaemia and Reperfusion,nt cellular oligopeptide with a thiol group. Glutathione, like other small peptides, is not generated by messanger RNA-directed ribosomal protein synthesis, but it is synthesized from free amino acids within each cell (2).
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Alterations in Membrane Phospholipids, Mechanisms of Free Radical Damage and Antioxidant Protectionr, it has become apparent that a major alteration in the integrity of cell membranes may be a critical event in the evolution of ischemic damage from a reversible to an irreversible condition. Several mechanisms capable of altering membrane biochemistry have been examined for their role in initiatin
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Xanthine Oxidase is not Likely to be a Source of Injurious Free Radicals in the Ischemic Human Hearsubject of current debate. Studies from this laboratory indicate that xanthine oxidase is an important source of cytotoxic free radicals in the reperfused dog heart (3). Xanthine oxidase can produce oxi-radicals by the following mechanism. During ischemia ATP in the myocyte is degraded through sever
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Role of Oxy-Radicals in Postischemic Myocardial Dysfunction,amental strategy in the management of acute ischemic syndromes in patients with coronary artery disease. The explosive growth of interventional recanalization, coupled with the widespread recognition that spontaneous reperfusion occurs commonly following coronary artery spasm or thrombosis, has prov
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Acute Effects of Antioxidants on in Vivo Models of Experimental Myocardial Ischemia and Infarction,by reduce the extent of ischemia-induced myocyte injury (1–3). However, it has more recently been suggested that reperfusion is a ‘double-edged sword’ (4): that is, restoration of blood flow may salvage some previously ischemic tissue, yet have deleterious effects on other previously ischemic myocyt
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