Myocardial ischemia and reperfusion: The role of oxygen radicals in tissue injury
dc.contributor.author | Werns, Steven W. | en_US |
dc.contributor.author | Lucchesi, Benedict Robert | en_US |
dc.date.accessioned | 2006-09-11T15:01:30Z | |
dc.date.available | 2006-09-11T15:01:30Z | |
dc.date.issued | 1989-01 | en_US |
dc.identifier.citation | Werns, Steven W.; Lucchesi, Benedict R.; (1989). "Myocardial ischemia and reperfusion: The role of oxygen radicals in tissue injury." Cardiovascular Drugs and Therapy 2(6): 761-769. <http://hdl.handle.net/2027.42/44595> | en_US |
dc.identifier.issn | 0920-3206 | en_US |
dc.identifier.issn | 1573-7241 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/44595 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=2488090&dopt=citation | en_US |
dc.description.abstract | Thrombolytic therapy has gained widespread acceplance as a means of treating coronary artery thrombosis in patients with acute myocardial infarction. Although experimental data have demonstrated that timely reperfusion limits the extent of infarction caused by regional ischemia, there is growing evidence that reperfusion is associated with an inflammatory response to ischemia that exacerbates the tissue injury. Ischemic myocardium releases archidonate and complement-derived chemotactic factors, e.g., leukotriene B 4 and C 5a , which attract and activate neutrophils. Reperfusion of ischemic myocardium accelerates the influx of neutrophils, which release reactive oxygen products, such as superoxide anion and hydrogen peroxide, resulting in the formation of a hydroxyl radical and hypochlorous acid. The latter two species may damage viable endothelial cells and myocytes via the peroxidation of lipids and oxidation of protein sulfhydryl groups, leading to perturbations of membrane permeability and enzyme function. Neutrophil depletion by antiserum and inhibition of neutrophil function by drugs, e.g., ibuprofen, prostaglandins (prostacyclin and PGE 1 ), or a monoclonal antibody, to the adherence-promoting glycoprotein Mo-1 receptor, have been shown to limit the extent of canine myocardial injury due to coronary artery occlusion/reperfusion. Recent studies have challenged the hypothesis that xanthine-oxidase-derived oxygen radicals are a cause of reperfusion injury. Treatment with allopurinol or oxypurinol may exert beneficial effects on ischemic myocardium that are unrelated to the inhibition of xanthine oxidase. Furthermore, the human heart may lack xanthine oxidase activity. Further basic research is needed, therefore, to clarify the importance of xanthine oxidase in the pathophysiology of reperfusion injury. Current data are highly suggestive of a deleterious role of the neutrophil in organ reperfusion and justify consideration of the clinical investigation of neutrophil inhibitors in patients receiving thrombolytic agents during the evolution of an acute myocardial infarction. | en_US |
dc.format.extent | 923243 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Kluwer Academic Publishers; Springer Science+Business Media | en_US |
dc.subject.other | Medicine & Public Health | en_US |
dc.subject.other | Cardiology | en_US |
dc.subject.other | Myocardial Ischemia | en_US |
dc.subject.other | Myocardial Infarction | en_US |
dc.subject.other | Reperfusion Injury | en_US |
dc.subject.other | Oxygen Free Radicals | en_US |
dc.subject.other | Neutrophils | en_US |
dc.subject.other | Xanthine Oxidase | en_US |
dc.title | Myocardial ischemia and reperfusion: The role of oxygen radicals in tissue injury | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Chemistry | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Internal Medicine(Division of Cardiology), The University of Michigan Medical School, 48109, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Pharmacology, The University of Michigan Medical School, 48109, Ann Arbor, Michigan; Department of Pharmacology, The University of Michigan Medical School, 6322 Medical Science Building I, 48109-0626, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 2488090 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/44595/1/10557_2004_Article_BF00133206.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF00133206 | en_US |
dc.identifier.source | Cardiovascular Drugs and Therapy | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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