Mechanisms of postischemic contractile dysfunction. Ann Thorac Surg 1999 Nov;68(5):1898-904
Date
12/10/1999Pubmed ID
10585101DOI
10.1016/s0003-4975(99)01035-8Scopus ID
2-s2.0-0032711491 (requires institutional sign-in at Scopus site) 101 CitationsAbstract
Prolonged reversible postischemic contractile dysfunction that follows single or multiple brief periods of regional or global ischemia has been termed "stunned myocardium," and is thought to be the result of a decreased responsiveness of the cardiac myofilaments to calcium. A number of hypotheses have been proposed to explain the pathogenesis of stunned myocardium; however, the two major theories that are supported by the most experimental evidence suggest that the generation of oxygen-derived free radicals and a disturbance in calcium homeostasis are responsible for the postischemic contractile dysfunction observed. These mechanisms are not mutually exclusive, and data are available that support both theories. Evidence exists that indicates that one may pharmacologically enhance the recovery of stunned myocardium by use of oxygen radical scavengers, adenosine agonists, calcium channel blockers, and openers of the ATP-sensitive potassium channel, including the volatile anesthetic isoflurane. Ischemic preconditioning (IPC) has also been shown to produce delayed protection against myocardial stunning, and a novel pharmacological agent, monophosphoryl lipid A, has been shown to mimic the effect of IPC. Because stunning appears to occur in a number of clinical settings, it is important to understand the mechanisms involved and to develop pharmacological therapy that will result in an improved clinical outcome.
Author List
Gross GJ, Kersten JR, Warltier DCMESH terms used to index this publication - Major topics in bold
AnimalsCalcium
Humans
Ion Channels
Ischemic Preconditioning, Myocardial
Myocardial Contraction
Myocardial Ischemia
Myocardial Reperfusion Injury
Myocardial Stunning
Reactive Oxygen Species
