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Cardiac reperfusion damage prevented by a nitroxide free radical.

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Cardiac reperfusion damage prevented by a nitroxide free radical.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gelvan, D. Saltman, P. Powell, S. R.
Description	Author Affiliation: Gelvan D ( Department of Biology, University of California, San Diego, La Jolla 92093.);
Abstract	Experimental evidence is presented that directly links ischemia/reperfusion injury to the formation of oxygen-derived free radicals. 2,2,6,6-Tetramethylpiperidine-N-oxyl (TEMPO)--a stable nitroxide radical that disproportionates superoxide radicals and oxidizes reduced metal ions required for OH. formation--was tested for its ability to prevent reperfusion damage in the isolated rat heart subjected to regional ischemia. Severe reperfusion arrhythmia--ventricular fibrillation and ventricular tachycardia--were prominent in control hearts, and their duration was significantly reduced by the presence of 0.4 or 1 mM TEMPO. TEMPO also repressed both postischemic release of lactate dehydrogenase and OH. formation. TEMPO slowed the heart rate, but compensatory pacing did not alter the dramatic effect of the nitroxide on reperfusion arrhythmia. TEMPO was partially protective when introduced at the end of ischemia but had no effect when added 1 min into reperfusion. It was concluded that both reperfusion arrhythmia and cell damage were directly related to oxidative damage incurred during the critical first minute of reperfusion. TEMPO strongly protected against reperfusion injury by preventing the formation of OH. and not by decreasing heart rate or by direct suppression of arrhythmia.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	11
Volume Number	88
Language	English
Publisher	National Academy of Sciences
Publisher Date	1991-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Arrhythmias, Cardiac Prevention & Control Cyclic N-Oxides Pharmacology Myocardial Reperfusion Injury Animals Etiology Physiopathology Biological Markers Free Radicals Heart Drug Effects Physiology Hydroxides Hydroxyl Radical In Vitro Techniques Kinetics L-Lactate Dehydrogenase Myocardial Reperfusion Rats, Inbred Strains Time Factors Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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