title: Role of oxygen in postischemic myocardial injury.
abstract: 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.affiliation: Department of Internal Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA.
authors.forename: Vijay Kumar
authors.initials: VK
authors.lastname: Kutala
authors.forename: Mahmood
authors.initials: M
authors.lastname: Khan
authors.forename: Mark G
authors.initials: MG
authors.lastname: Angelos
authors.forename: Periannan
authors.initials: P
authors.lastname: Kuppusamy
mesh_terms: D000818:Animals; D017209:Apoptosis; D005609:Free Radicals; D006801:Humans; D000860:Hypoxia; D020935:MAP Kinase Signaling System; D009682:Magnetic Resonance Spectroscopy; D017202:Myocardial Ischemia / Q000473:pathology; D015428:Myocardial Reperfusion Injury; D009206:Myocardium / Q000473:pathology*; D009569:Nitric Oxide / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism*; D010102:Oxygen Inhalation Therapy; D015427:Reperfusion Injury; D013997:Time Factors
chemical_list: D005609:Free Radicals; D009569:Nitric Oxide; D010100:Oxygen