title: Reperfusion injury: a review of the pathophysiology, clinical manifestations and therapeutic options.
abstract: Lack of blood supply or ischaemia underlies many of the most important cardiovascular and cerebrovascular diseases faced by clinicians in their daily practice. Many of these ischaemic episodes can be reversed at an early stage by surgical or pharmacological means with the ultimate aim of preventing infarction and cell necrosis in the ischaemic tissues. However, reperfusion of ischaemic areas, in particular the readmission of oxygen, may contribute to further tissue damage (reperfusion injury). For example, the use of thrombolytic therapy in acute myocardial infarction and other revascularisation procedures, such as percutaneous transluminal angioplasty and coronary artery bypass surgery, may be associated with reperfusion of ischaemic myocardium. Such ischaemia and reperfusion may result in injury to one of more of the biochemical, cellular and microvascular components of the heart. Our understanding of the significance of reperfusion injury is however restricted by the profuse literature in animal models and limited literature in the clinical situation. This article reviews the pathophysiology, clinical manifestations of reperfusion injury to the heart and discusses the possible therapeutic approaches to avoiding any adverse effects.
authors.affiliation: Division of Clinical Pharmacology, Leicester Royal Infirmary, UK.
authors.forename: S R
authors.initials: SR
authors.lastname: Maxwell
authors.forename: G Y
authors.initials: GY
authors.lastname: Lip
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology; D015415:Biomarkers; D002118:Calcium; D004195:Disease Models, Animal; D005609:Free Radicals; D006801:Humans; D017202:Myocardial Ischemia / Q000150:complications / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology* / Q000517:prevention & control*; D017682:Myocardial Stunning / Q000209:etiology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D010086:Oxidative Phosphorylation Coupling Factors / Q000502:physiology
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D005609:Free Radicals; D010086:Oxidative Phosphorylation Coupling Factors; D002118:Calcium