title: Pharmacological possibilities for protection against myocardial reperfusion injury.
abstract: Reperfusion through thrombolysis or percutananeous coronary angioplasty is standard treatment in impending acute myocardial infarction. Although restoration of blood flow to the jeopardised myocardial area is a perquisite for myocardial salvage, reperfusion itself may lead to accelerated and additional myocardial injury beyond that generated by ischemia alone. This is referred to as the "reperfusion injury". Since the reperfusion injury is initiated by the treatment of myocardial infarction, it is of importance to limit the extent of the injury. Several studies aimed at preventing reperfusion injury by means of pharmacological agents have therefore been conducted. The design of such studies is crucial for the results. Factors of importance are the timing of drug administration, animal species used, the degree of collateral flow and the duration of ischemia. A variety of pharmacological compounds have been investigated in different experimental models of myocardial ischemia and reperfusion. These include oxygen free radical scavengers, antioxidants, calcium channel blockers, inhibitors of neutrophils, nitric oxide, adenosine-related agents, inhibitors of the renin-angiotensin system, endothelin receptor antagonists, Na(+)/H(+) exchange inhibitors, and anti-apoptotic agents. All these groups of pharmacological agents have been demonstrated to protect from reperfusion injury determined as limitation of infarct size, improved myocardial and endothelial function, and reduced incidence of arrhythmias. The mechanism behind the protective effect may differ between different groups of compounds, but some compounds may exert cardioprotection via common pathways. Such a pathway may be via maintained bioavailability of nitric oxide.
authors.affiliation: Department of Integrative Pharmacology, AstraZeneca R&D, Mölndal, Sweden.
authors.forename: Qing-Dong
authors.initials: QD
authors.lastname: Wang
authors.forename: John
authors.initials: J
authors.lastname: Pernow
authors.forename: Per-Ove
authors.initials: PO
authors.lastname: Sjöquist
authors.forename: Lars
authors.initials: L
authors.lastname: Rydén
mesh_terms: D000241:Adenosine / Q000819:agonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D065128:Endothelin Receptor Antagonists; D016166:Free Radical Scavengers / Q000627:therapeutic use; D006801:Humans; D023421:Models, Animal; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D020556:Neutrophil Infiltration / Q000187:drug effects; D009569:Nitric Oxide / Q000627:therapeutic use; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000975:Antioxidants; D002121:Calcium Channel Blockers; D065128:Endothelin Receptor Antagonists; D016166:Free Radical Scavengers; D017923:Sodium-Hydrogen Exchangers; D009569:Nitric Oxide; D000241:Adenosine