Document Detail


Role of oxygen in postischemic myocardial injury.
MedLine Citation:
PMID:  17571958     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Myocardial function is dependent on a constant supply of oxygen from the coronary circulation. A reduction of oxygen supply due to coronary obstruction results in myocardial ischemia, which leads to cardiac dysfunction. Reperfusion of the ischemic myocardium is required for tissue survival. Thrombolytic therapy, coronary artery bypass surgery and coronary angioplasty are some of the treatments available for the restoration of blood flow to the ischemic myocardium. However, the restoration of blood flow may also lead to reperfusion injury, resulting in myocyte death. Thus, any imbalance between oxygen supply and metabolic demand leads to functional, metabolic, morphologic, and electrophysiologic alterations, causing cell death. Myocardial ischemia reperfusion (IR) injury is a multifactorial process that is mediated by oxygen free radicals, neutrophil activation and infiltration, calcium overload, and apoptosis. Controlled reperfusion of the ischemic myocardium has been advocated to prevent the IR injury. Studies have shown that reperfusion injury and postischemic cardiac function are related to the quantity and delivery of oxygen during reperfusion. Substantial evidence suggests that controlled reoxygenation may ameliorate postischemic organ dysfunction. In this review, we discuss the role of oxygenation during reperfusion and subsequent biochemical and pathologic alterations in reperfused myocardium and recovery of heart function.
Authors:
Vijay Kumar Kutala; Mahmood Khan; Mark G Angelos; Periannan Kuppusamy
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  9     ISSN:  1523-0864     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-07-20     Completed Date:  2007-09-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1193-206     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia
Apoptosis
Free Radicals
Humans
MAP Kinase Signaling System
Magnetic Resonance Spectroscopy
Myocardial Ischemia / pathology
Myocardial Reperfusion Injury
Myocardium / pathology*
Nitric Oxide / metabolism
Oxygen / metabolism*
Oxygen Inhalation Therapy
Reperfusion Injury
Time Factors
Chemical
Reg. No./Substance:
0/Free Radicals; 10102-43-9/Nitric Oxide; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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